GI Patho Flashcards
GERD Etiology
- Decrease LES tone
- anticholinergics
- nicotine - Increased intra-abdominal pressure
- obesity
- pregnancy - decreased motility
- gastroparesis
GERD Pathophysiology
- Reflux gastric contents into esophagus
- HCl acid
- pepsin
- bile salts - Direct irritation of esophageal mucosa
- Inflammatory response
- erythema
- Increase vascular permeability, edema
- esophageal erosions
- Barrett’s esophagus - Adenocarcinoma
GERD
Clinical manifestations
Pyrosis (heart burn)
Dyspepsia
Dysphagia
Pain (worse lying down, after eating)
Cough
Laryngitis
Worsening asthma
GERD
Pharmacological treatment
PPI - omeprazole
H2 receptor antagonists - cimetidine
antacids - calcium carbonate
pro kinetic agents - metoclopromide
GERD
Non-pharmacological treatment
- LES sphincter
- stop smoking (nicotine) - Intraabdominal pressure
- lose weight
- lose clothing
- HOB elevated - GI motility
- walking after eating
- staying upright
GERD
Diagnosis
- physical assessment
- clinical history
- endoscopy with biopsy (r/o eosinophilic esophagitis)
- R/O cardiac (angina? MI?)
Two types of GERD
- erosive
- non-erosive (heart burn, no esophageal injury)
Gastritis
Definition
Inflammation of the stomach
- Acute
- Chronic (1. autoimmune type A ; 2. chronic non-immune type B)
Acute Gastritis
Pathophysiology
Direct injurious agent
Damage and inflammation to superficial mucosa (fundus, antrum, both)
- Nicotine
- NSAIDs
- H. pylori
- histamine
- Alcohol
- Urea
- digoxin
Acute Gastritis
Treatment
H2 receptor blockers
Antacids
Remove injurious agent (D/C alcohol, smoking, NSAID etc.)
Self resolves in a couple of days
Chronic Gastritis
Pathophysiolgy
- Type A - autoimmune
- Antibodies against H/K ATPase
- destruction parietal cells
- no Intrinsic factor –> Vitamin B12 deficiency –> pernicious anemia
- no HCl - Type B - non-immune
- H. pylori infection (NSAIDs, smoking, alcohol)
- chronic inflammation -> damage
- HCl normal
- can lead to pan gastritis (autoimmune gastritis)
Chronic Gastritis
Clinical symptoms
Non-specific
epigastric pain
fullness
anorexia
N/V
fatigue
anemia
bleeding
Diagnosis
Chronic Gastritis
- physical examination
- history
- biopsy
- achlorhydria
- Intrinsic Factor
- Vitamin B12
- other autoimmune disorders - thyroid, RA, type I DM
Treatment
Chronic Gastritis
H. pylori
- quadruple / triple antibiotic therapy
D/C causative agent
- D/C NSAIDs, smoking, alcohol
- if non-immune
Rx
- Vitamin B12 if autoimmune
- iron supplmentation
Small regular meals
Risk Factors
Peptic Ulcer Disease
NSAIDS
H. pylori infeciton
Chronic diseases (emphysema, RA, cirrhosis, obesity, diabetes)
Age
Smoking
Alcohol
Stress
Type O blood
Defintion
Peptic Ulcer Disease
Erosion (superficial - mucosal layer) / ulceration (deep - muscularis) of the mucosal lining of
1. esophagus
2. stomach
3. duodenum
Complications
Peptic Ulcers
- Hemorrhage
- perforation
- obstruction
Zollinger-Ellison Syndrome
PUD
Tumor secretes gastrin
Gastrin
hormone secreted by G cells (stomach, duodenum)
increase HCl secretion
increase GI motility
Etiology
Duodenal ulcers
most common ulcer
1. H. pylori
2. NSAIDS
3. idiopathic (rare)
Pathophysiology
Duodenal Ulcer
NSAID
Trigger (NSAID, H. pylori) –> acid/pepsin in duodenum –> penetration mucosal barrier –> erosion –> ulceration
NSAID
direct irritant, damage mucosal lining
also decrease mucous secretion, bicarbonate secretion, and blood flow to the mucosal barrier
Pathophysiology
Duodenal Ulcer
H. Pylori
H. pylori
urease - neutralizes pH, decrease viscosity mucous
Cag A virulence factor - elongation epithelial cells, disruption tight junction
Cag A immunogenic –> inflammation, infiltration
VacA virulence factor - pores, vacuolation, apoptosis
VacA virulence factor –> inhibit proliferation T cells, apoptosis T cells –> adaptive immune evasion
Change flagella –> evade TLR recognition innate immune system
Clinical manifestations
Duodenal ulcer
NSAID
- asymptomatic
- painless hemorrhage and perforation
- melena stool
- hematemesis
- anemia
H. pylori
- chronic intermittent epigastric pain
- urea breath test
- wakes up at night
- nocturnal pain
- relieved with eating (reoccurs 2-3 hours after eating)
- pain - antacid/food- relief pattern
- anemia
- remission to relapse
- heals more quickly
Pharmacological Treatment
Duodenal ulcers
H. pylori
- quadruple therapy (metronidazole + tetracycline + bismuth + PPI)
- triple therapy (metronidazole/amoxicillin + clarithromycin + PPI)
- antacids (calcium carbonate, aluminum hydroxide, magnesium hydroxide, sodium bicarbonate)
- H2 receptor antagonists (cimetidine, famotidine, ranitidine)
- PPI (omeprazole, lansoprazole)
- Sucrafalate (ulcer protection)
NSAID
- D/C NSAID
- PPI (omeprazole, lansoprazole)
- H2 receptor antagonist (cimetidine, famotidine)
- antacids
- sucrafalate
Pathophysiology
Gastric Ulcers
Break in mucosal barrier
- NSAID ( no prostaglandins )
- H. pylori infection ( virulence factors, urease)
- reflux from SI (bile, pH, mucous viscosity decrease)
- decreased parietal cells (chronic gastritis)
- decrease mucus production
Exposure epithelium to H+ and pepsin –> erosions
Clinical Symptoms
Gastric Ulcers
intermittent epigastric pain
pain when food in stomach
pain- antacid-relief pattern
chronic ulcer without remission
heals more slowly
more weight loss, vomiting, anorexia
Diagnosis
Gastric Ulcers
- physical examination
- history
- endoscopy with biopsy
- gastrin to r/o cancer
- urea breath test, H. pylori stool test
Treatment
Gastric ulcer
- PPI
- H2 receptor antagonist
- Antacid
- Antibiotic if H. pylori (quadruple or triple therapy)
- sucrafalate
Pathophysiology
Stress Ulcers
Physiological stress (multi-system trauma, TBI, sepsis, ventilation > 48 hours) –> activation SNS –> vasoconstriction –> ischemia –> decreased blood flow to GI mucosal barrier –> disruption barrier –> exposure H+ and pepsin –> erosions, ulceration
Cushing ulcer
Treatment
Stress ulcers
prophylactic treatment
PPI
H2 receptor antagonists
Cellular pathophysiology
Gastric ulcers
- abnormal mucus
- normal/low parietal cell mass
- normal/low acid production
- high gastrin
- normal pepsinogen
- H. pylori 80%
Cellular pathophysiology
duodenal ulcers
- abnormal mucus
- high parietal cells
- high acid production
- normal gastrin
- high pepsinogen
- H. pylori 95-100% time
Pathophysiology
PUD
Trigger (NSAID, h. pylori, alcohol, smoking, schema)
Disruption mucosal barrier
- decrease mucus
- decrease tight junctions
- gastric acid direct contact with mucosa
Conversion pepsinogen to pepsin
- erosion
Histamine
- vasodilation, permeability, edema, pain, infalmmation
- increase acid secretion
- erosions
- muscle spasms (acid)
Infantile Hypertrophic Pyloric Stenosis
Pathophysiology
Narrowing of pyloric sphincter (ingrowth of muscles) prevents food from passing from stomach to small intestine
Hypertrophic pyloric stenosis
Clinical Signs and Symptoms
projectile vomiting
palpable olive mass RUQ
demands to be re-fed
weight loss
occurs 2-8 weeks neonate
Hypertrophic pyloric stenosis
Treatment
Laparoscopic pyloromyotomy
Paediatric
Gastric Esophageal reflux
Normal for first 12 months?
True
Paediatric GERD
Clinical Manifestations
food refusal
dysphagia
epigastric pain
wheezing
sinusitis, pharyngitis, otitis media
Paediatric GERD
Treatment
R/O milk allergy
endoscopy with biopsy R/O barren esophagus and adenocarcinoma
pro kinetics - metoclopromide
feed - thicken
Paediatric GERD
Causes
LES sphincter tone low
anatomy
Cells and secretions
Stomach
Chief cells - pepsinogen
mucousal cells - gastrin
D cells - somatostatin
Enterocromaffen cells - histamine
parietal cells - HCl
Stimulation secretions
Acetylcholine
- stimulates Gastrin
- pepsinogen
- HCl
Gastrin
- stimulates histamine
- HCl
- pepsinogen release
Histamine
- stimualtes HCl release
Prostaglandins/NO
- protective of mucosal barrier
- increase mucous, bicarb, and decrease HCl secretions
