Stomach Disorders: Hiatal Hernia and Gastritis

stomach, diaphragm, aging

Hiatal Hernia: Background

-Protrusion (herniation) of the upper part of the _______ through the ___________ into the thorax

-Risk Factors → obesity, _____, and weakening of musculofascial structures. Really anything that causes a loss of elasticity

GE, above, short, vagal, muscles, supine, down, pressure, reflux, LES

Type 1: Sliding Hernia (MC)

-__ junction slides _____ diaphragm with some of the stomach

-Could be due to a congenitally _____ esophagus, fibrosis or excessive _____ nerve stimulation, or weakening of the diaphragmatic ________ at the GEJ contributes

-______ position causes hernia to slide up and standing causes it to slide ______

-Exacerbated by increased intraabdominal ___________ secondary to coughing, bending, tight clothing, obesity, etc.

-Associated with ______ (diminishes resting pressure of ___)

rolling, fundus, esophagus, below, reflux, ulcer, ischemia

Type II: Paraesophageal Hernia (________ hernia)

-Herniation of the gastric ______ alongside the ___________, with the GEJ remaining _____ the diaphragm

-______ is uncommon because the sphincter mechanism is intact

-Can cause congestion of mucosal blood flow leading to gastritis and ______

-Strangulation can occur, causing __________ and necrosis

GERD, III, viscera

Hiatal Hernia: Type III and IV

-Type III → Mixed Hernia

• Combo of type I and II

• Occur in conjunction with other diseases like ____, peptic ulcer, cholecystitis

-Type IV

• Aggravated form of Type ___

• Includes herniation of other abdominal ________ (intestine, pancreas, spleen)

asymptomatic, heartburn, pain, fullness, bleeding

Hiatal Hernia Symptoms

-MC in Type I and III:

• Often ____________

• ________

• Regurgitation

• Dysphagia

-MC in Type II-IV:

• Epigastric or substernal ____

• Postprandial ___________

• N/V

-Strangulation Symptoms → acute, severe chest/epigastric pain, N/V, GI ________

thorax, swallow, hernia, GE

Hiatal Hernia: Diagnosis

-CXR → see protrusion of stomach into the ______, often found incidentally

-Barium ________ → determine anatomy and size of ______, orientation of stomach, location of GE junction

-Upper endoscopy

-Manometry → shows location of __ junction

GERD, prophylactic, repair, below, fundoplication

Hiatal Hernia: Treatment

-Type I

• Asymptomatic → nothing

• Symptomatic → manage ____ (PPI, weight loss if needed)

-Type II-IV

• Asymptomatic → controversial, most are against ____________ surgical intervention

• Symptomatic → surgical _____. Return herniated stomach _______ diaphragm, repair enlarged esophageal hiatus, and then ____________

inflammatory, mucosa, NSAIDs, shock, H. pylori, autoimmune

Gastritis: Background

-Acute or chronic ____________ disorder of the gastric ______

-Subtypes:

• Erosive → _______ or ETOH, MC cause of acute gastritis

• Reflux

• Hemorrhagic → reaction to hemodynamic disorder (_____)

• Infectious → _._____ or viruses

• Atrophic → _____________, environmental, and H.pylori can cause too

protective, NSAIDs, prostaglandin, hypermotility, ETOH, erosions

Acute Gastritis: Background

-Injury of the ____________ mucosal barrier (drugs, chemicals)

-_______ inhibit action of COX-1 → inhibit ___________ synthesis

-NSAIDs (not ASA) cause gastric ____________ → mucosal compression and injury

-_____, metabolic disorders (uremia) can contribute

-Superficial or deep ________ with or without hemorrhage

epigastric, bleeding, spontaneously

Acute Gastritis Symptoms

-Abdominal discomfort

-N/V

-__________ tenderness

-Gastric mucosal _________

-Heals ____________ within a few days

atrophy, metaplasia, fundal, antral, pangastritis

Chronic Gastritis: Background

-Chronic inflammation, mucosal _______, epithelial ___________ progressing over years

-Type A (immune, ______, associated with rheumatoid arthritis and T1D), Type B (nonimmune, _______, associated with H.pylori), Type AB (__________), and Type C

severe, T-cell, autoantibodies, parietal, mucosa, anemia, B12, autoimmune

Type A-Immune (Fundal) Gastritis

-Rare but most ______ form

-Associated with loss of _-____ tolerance and development of _____________ against _______ cells or intrinsic factor or both

-Gastric ______ degenerates significantly in body and fundus leading to atrophy

-Can lead to pernicious _______ (decreased vitamin ____ absorption)

-Associated with other _____________ disorders (RA, T1D)

H.pylori, mimicry, fundus, ETOH, NSAIDs

Type B-nonimmune (Antral) Gastritis

-More common

-Associated with _.______ infection

• May trigger immune response through molecular ________ or cause mucosal injury

• Can progress to autoimmune atrophic gastritis and involve ______ (Type AB)

-Chronic use of ____, tobacco, and _______ may contribute

anorexia, bleeding

Chronic Gastritis: Symptoms

-__________ → maybe associated weight loss

-Fullness

-N/V

-Epigastric pain

-Gastric mucosal ___________

negative, fecal-oral, asymptomatic, PUD, adenocarcinoma, increased, decreased

Helicobacter Pylori: Background

-Gram-________ rod with flagellum

-Transmitted by _____-____ or oral-oral route, usually acquired in childhood

-____________ in 70% of cases

-Gene-environment interaction and different strains increase risk of developing disease/symptoms

-Common cause of chronic/acute gastritis, ___, gastric _____________, gastric mucosa-associated lymphoid tissue (MALT)

• Causes inflammation, __________ gastric secretion in antral gastritis and _________ gastric secretion in fundal gastritis, pain, N/V

urease, ammonia, neutralizes, protective, penetration, epithelium, adhesion, cytokines, apoptosis

H.pylori: Pathogenic/Virulence Factors

-Bacterial ______ hydrolyzes gastric luminal urea to form ________, which __________ gastric acid and forms __________ cloud around organism. This enables ____________ of gastric mucus layer

-Spiral shape, flagella, and mucolytic enzymes produced facilitate passage through mucus layer to gastric __________

• Attaches to gastric epithelial cells by specific receptor mediated ________

-Release ___________ and chemokines, which promotes gastric epithelial cell ____________

• Results in atrophy, ulcers, cell proliferation/dysplasia/cancer

60, NSAIDs, iron, peptic

H.pylori: Indications for Testing

-Pts with dyspepsia < __ y/o who do not have alarm symptoms

-Prior to chronic treatment with ________

-Unexplained _____ deficiency

-Adults with immune thrombocytopenia

-MALT

-Active or PMH of _______ ulcer

-Early gastric cancer

endoscopy, urease, breath, CO2, stool

H.pylori: Diagnosis

-Upper ___________ (gold standard) → biopsy ______ test, tissue histology, C&S of biopsied specimens

• Rapid urease test is positive when there is a change in the pH and color of test material. Taking antacid therapy within a wk before testing can give false negatives

-Urea _____ test → based on hydrolysis of urea by H. pylori to produce ___ and ammonia

-______ antigen assay → detect bacterial antigens

-Serologic Testing → IgG/IgM are the least sensitive tests (elevated within 2mo or 3-4 wks of infection), used to support diagnosis

metronidazole, tetracycline, PPI, amoxicillin, confirm, after

H. pylori: Treatment

-Quadruple therapy (1st line) → bismuth subsalicylate + ____________ + __________ + ___

• Given for 10-14 days

-Triple therapy (old 1st line) → PPI + ___________ + clarithromycin

• Given for 14 days

-_______ eradication (4+ weeks after treatment) → urea breath test, stool antigen test, or endoscopy

stop, H2, PPI, H.pylori

Gastritis: Treatment

-____ offending drug/chemical (NSAIDs or ETOH)

-Antacids

-__ receptor antagonists

-___ x 8-12 weeks

-Treat _._____ if present