Upper GI Problems Flashcards
What is a esophageal disorder?
GERD
Gastro-Esophageal Reflux Disease (GERD)
Is a syndrome; not a disease
Most prevalent acid-related disorder
Cause is multi-factorial
Results when defences of lower esophagus are overwhelmed by reflux of stomach acidic contents into esophagus → results in irritation and inflammation
One of the primary factors → incompetent lower esophageal sphincter (LES)
A common cause → hiatal hernia
Clinical Manifestations of GERD
Diagnosis based on history and physical exam
Heart burn (pyrosis) → most common
- From gastro-esophageal reflux
- Burning, tight sensation, intermittently beneath lower sternum, radiating to throat and jaw
- After ingestion of food that ↓ LES pressure
Regurgitation
Dysphagia
Odynophagia (painful swallowing
Plus, more (see textbook)
IMPORTANT NOTE: re: further investigation
What is the difference between MI and GERD
lab values
Complications of GERD
Related to direct exposure of gastric acid on esophageal mucosa:
Esophagitis
- Scar tissue formation & ↓ distensibility from repeated exposure
Barretts esophagus (cells of intestines)
- Considered a precancerous lesion, ↑ risk for esophageal cancer
- Endoscopic monitoring Q2-3 years
respiratory complications: bronchospasm, laryngospasm, cricopharyngeal spasm
DX of GERD
Barium swallow studies - swallow barium and then it follows when you swallow. Is the esophageal sphincter working properly?
Endoscopy
Esophageal nanometric studies - finds out pressure in sphincter
Radionuclide tests
Care of GERD
Lifestyle modification
- Attention to diet & drug that affect LES, acid secretion, or gastric emptying
- Obese patients are encouraged to lose weight
- Smokers are encouraged in smoking cessation
Nutritional therapy
- Food can aggravate symptoms
- Foods causing reflux:
Fatty foods (release cholecystokinin)
High fat foods
- Foods that ↓ LES pressure should be avoided
- Encourage small frequent meals
Drug therapy
- Goals: improve lower esophageal function, ↑ esophageal clearance, ↓ vol and acidity of reflux, & protect esophageal mucosa
What are the 2 approaches of drug therapy
“step-up” approach (less severe drugs – start with antacid, H2 blocker, then PPI)
“step down” approach (start with more severe drugs, then go down to antacids)
a) Antisecretory agents
b) PPIs
- promotes esophageal healing
c) Cholinergic drugs
- ↑ LES pressure, ↑esophageal emptying, ↑ gastric emptying
Disorders of the stomach and Duodenum
Gastritis
Peptic Ulcer Disease
Gastric Ulcers
Duodenal Ulcers
2 types of gastritis
Acute
Chronic
- autoimmune
- diffuse antral (lower part of the stomach)
multifocal
Patho of gastritis
Result of breakdown in normal gastric mucosal barrier
HCl can diffuse back into mucosa
Results in tissue edema, disruption of capillary walls with loss of plasma
into gastric lumen, possibly hemorrhage
Causes of gastritis
Drugs
- ASA, NSAIDS (advil), steroids : directly irritating and inhibit prostaglandin synthesis
Dietary indiscretions
- Alcoholic drinking binge – destruction of epithelial cells, mucosal congestion, edema, hemorrhage
- a large quantities of spicy, irritating foods
Microorganisms
- H. pylori
H. pylori
Capable of breakdown of gastric mucosal barrier with a “trigger”
Chronic gastritis, in diffuse, antral, and multifocal types
Don’t have symptoms of gastritis
Bacteria, viruses and fungi (ie Mycobacterium, CMV, Treponema pallidum)
Clinical manifestations of acute gastritis
Anorexia
N/V
Epigastric tenderness
Feeling of fullness
hemorrhage can occur with alcohol abuse
Lasts a few hours to a few days
Self –limiting- mucosa is expected to heal in a few days.
Clinical manifestations of chronic gastritis
Some have no symptoms
Acid-secreting cells eventually lose their function atrophy → loss of intrinsic factor (essential for absorption of cobalamin(Vit B12), which is needed for growth and maturation of RBC) results in deficiency
Over time, anemia and neurological complications can occur.
Care of Acute gastritis
Eliminate the cause
Prevent the cause in the future
If vomiting →
If severe → N/G, to lavage precipitating agent or suction
Drug therapy:
- to reduce irritation of gastric mucosa
- Relief of symptoms
Care of chronic gastritis
Eliminate cause
- Cessation of alcohol
- Abstinence from drugs
- H.pylori eradication → combination of abx and antisecretory agent
- For pernicious anemia- cobalamin tx
Lifestyle changes
- Non-irritating diet, in small meals
- No smoking
Strict adherence to meds
Adherence important can lead to gastric cancer.
Peptic Ulcer Disease (PUD)
Characterized by erosion of GI mucosa, resulting from digestive action of HCl acid and pepsin.
Types of PUD
Acute
Chronic
Based on:
Degree and duration of mucosal involvement
Location
Gastric and Duodenal
Stomach Erosion and Peptic Ulcer Stages - acute ulcers
Superficial erosion
Minimal inflammation
Of short duration
Resolves quickly when cause is removed
Stomach Erosion and Peptic Ulcer Stages - Chronic ulcers
Long duration
Erosion through muscular wall
Formation of fibrous tissue
Continually present for many months, or intermittently throughout lifetime
Patho of PUD
Stomach protected by gastric mucosal barrier
Surface mucosa of stomach renewed q3 days
Tissue injury caused by HCl leads to release of histamine → vasodilation & ↑ capillary permeability → histamine stimulates further secretion of acid and pepsin
Destructive agents: H. Pylori, ASA, NSAIDS, corticosteroids some chemo meds.
With mucosal barrier disruption, comes increased blood flow. If blood flow insufficient, tissue injury occurs.
Gastric ulcers
Most common sites: lesser curvature close the antral junction.
Less common and higher mortality than duodenal ulcers.
More prevalent in women and older adult.
Critical pathological process → amount of acid that penetrates mucosal barrier
Role of H. pylori → gastric mucosal destruction by drugs or smoking may be enhanced by H. pylori
Drugs: ASA, NSAIDS, corticosteroids
- Can cause acute gastritis, and sometimes lead to chronic ulcers
1-3% pts taking NSAIDS for 1 year experience serious GI complications such as gastric ulcer, upper GI hemorrhage, or ulcer perforation.
Positively linked to smoking
Duodenal Ulcers
80% of all peptic ulcers.
More men than women, but the trend is reversing
High incidence between 35-45 years.
Associated with high HCl secretion.
- High correlation with: COPD, cirrhosis, chronic pancreatitis, Chronic Renal Failure.
- Alcohol ingestion & heavy smoking- known to stimulate acid production
H. pylori plays a key role.
- Survives a long time in upper Gi because it has ability to move in mucus and attach to mucosal cells.
- Secretes urease → buffers area around bacterium and protects destruction in acidic environment.
- Found in 90-95% of patients with duodenal ulcers.
- Infection is thought to occur during childhood: fecal-oral or oral-oral.
Genetic etiology: persons with blood group O have increased incidence
Clinical manifestations of duodenal ulcers
Common for pts with PUD to have no pain or other symptoms.
When pain does occur/
- With duodenal ulcer, “burning”, “cramp-like”, mid-epigastric below xiphoid process
- With gastric ulcer, high epigastric, 1-2 hrs after meals, “burning”, “gaseous”
If ulcer has eroded through gastric mucosa, food makes it worse.
Ulcers located in posterior duodenum → back pain
Duodenal ulcer: occur continuously for a few weeks or months, then disappears for a time, only to recur some months later.
Complications of chronic PUD
1) Hemorrhage
- Most common.
- Higher in duodenal ulcers than gastric ulcers.
2) Perforation
- Most lethal.
- Common in large penetrating duodenal ulcers that have not healed.
- Spillage of gastric or duodenal contents into peritoneal cavity.
- Sudden and dramatic onset of severe pain across abdomen.
Rigid and board-like abdomen
Absent BS
Shoulder pain because of irritation to the phrenic nerve
3) Gastric outlet obstruction
- Increase in force needed to empty stomach → results in hypertrophy of stomach wall.
- A long history of ulcer pain.
- Involuntary vomiting, often projectile, common.
Non-invasive Diagnostic studies to confirm H. Pylori infection
Serum/ whole blood antibody tests
Urea breath test
Barium studies
Lab tests (CBC,LFTs, FOB)
Invasive diagnostic studies that confirm a H.Pylori Infection
Biopsy of the stomach- rapid urease test
Greater sensitivity and specificity than non-invasive methods but can’t be done without endoscopy
Conservative therapy for PUD
Aim: ↓ degree of gastric acidity
- Adequate rest
- Medication therapy- adherence until completely healed important
- Elimination of smoking
- Nutritional therapy
- eliminate alcohol and caffeine-containing products
- avoid spicy, pepper, carbonated drinks, tea, coffee and broth (meat).
Pain disappears after 3-6 days
Ulcer healing up to 3-9 weeks
Drug therapy for PUD
A vital part of therapy!
Strict adherence is important.
- Histamine-2 receptor (H2R) blockers. (ie. Famotidine)
- Proton pump inhibitors (ie. Pantoprazole)
- Antibiotics (ie. Amoxicillin, Clarithromycin) – if infection, with H. pylori
- Antacids (ie. Aluminum carbonate)
- Anticholinergics (ie.
↓ vagal stimulation of HCl secretion
Do not use in gastric ulcers
- Cytoprotective drug therapy (ie Misoprostol, Sucralfate)
Sx therapy for PUD
Uncommon
Treatment for complications or Gastric Ca
Surgeries:
- Partial gastrectomy
Vagotomy
- Pyloroplasty
Complications of Surgery
- Dumping Syndrome – vagal symptoms (weakness, sickness, abdo cramps, defecation)
- Postprandial Hypoglycemia – 3 hours after eating, flushing, tachycardia, diarrhea
- Bile Reflux Gastritis – damages esophagus
Post op care for PUD
Nutritional Therapy
Stomach size is reduced
Meal size must be reduced
No fluid with meals
Dry foods, low carb content, mod protein and fat content are best to minimize dumping syndrome
Rest periods after each meal x 30 mins in recumbent position
Unpleasant symptoms are short in duration
