Upper GI Problems Flashcards
Gastro-Esophageal Reflux Disease (GERD)
a syndrome, not a disease
the most prevalent acid-related disorder
Cause of GERD
- 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
- a common cause -> haital hernia (when the upper part of the stomach pushes up through the diaphragm)
One of the primary factors in GERD
Incompetent lower esophageal sphincter (LES)
How is GERD diagnosed
Diagnosis based on history and physical exam
Clinical Manifestations of GERD (7)
- heartburn (pyrosis) - most common
- burning, tight sensation, intermittently beneath lower sternum, radiating to throat and jaw
- after ingestion of food that decreased LES pressure
- regurgitation
- Dysphagia
- Odynophagia (painful swallowin)
- Requires further investigation to rule out MI because the symptoms can be similar.
Complications of GERD (3)
- Esophagitis
- Barretts esophagus
- Respiratory complications: bronchospams, laryngospasm, cricopharyngeal spasm
Esophagitis
Scar tissue formation & decreased distensibility from repeated exposure
Barretts esophagus
Considered a precancerous lesion, increased risk for esophageal cancer
Endoscopic monitoring Q2-3 years
Cells that look like large and small intestine cells are found in the esophagus
Diagnostic Studies for GERD
Barium swallow studies
Endoscopy
Esophageal nanometric studies (measures the pressure in the esophagus and sphincter)
Radionuclide tests
Collaborative Care 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
Collaborative Care GERD: Nutritional Therapy
- Food can aggravate symptoms
- Foods causing reflux (high fat foods)
- Foods that decreased LES pressure should be avoided: chocolate, peppermint, caffeine
- Encourage small frequent meals
Collaborative Care GERD: Drug Therapy Goal
- Goals: improve LES function, increased esophageal clearance, decreased vol and acidity of reflux & protect esophageal mucosa
Collaborative Care GERD: Drug Therapy - step-up approach vs step-down approach
step-up: Starts with nonprescription meds (antacids, and OTC histamine H2-receptor blockers; then prescription H2R blockers and finally proton pump inhibitors)
Step down: starting with a PPI and over time, titrating down to prescription H2R blockers and finally to OTC H2R blockers and antacids.
Collaborative Care GERD: Drug therapy - cholinergic drugs
- increased LES pressure, increase esophageal emptying, and increase gastric emptying
What is gastritis?
Inflammation of the gastric mucosa
Categories of Gastritis
- acute or chronic
- diffuse or localized
Subtypes of Chronic Gastritis
Autoimmune (involves the body and the funds of the stomach)
Diffuse Antral (affects primarily the antrum
Multifocal (diffse throughout the stomach
Pathophysiology of Gastritis
- result of breakdown in normal gastric mucosal barrier -> HCl can diffse back into the mucosa -> results in tissue edema, disruption of capillary walls with loss of plasma into gastric lumen, possibly hemorrhage
Causes of Gastritis: Drugs
- ASA, NSAIDS, corticosteroids, directly irritating and inhibit prostaglandin synthesis
Causes of Gastritis: Dietary indiscretions
Alcoholic drinking binge - destruction of epithelial cells, mucosal congestion, edema, hemorrhage
A large quantities of spicy, irritating foods
Causes of Gastritis: Microorganisms
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
Clinical Manifestations of Acute Gastritis (7)
- Anorexia
- N/V
- Epigastric tenderness
- Feeling of fullness
- hemorrhage 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 (3)
- Some have no symptoms
- progressive gastric mucosal atrophy from chronic alterations in the protective mucosal barrier causes the gastric chief and parietal cells to die eventually.
- Acid-secreting cells eventually lose their function and 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
Nursing Management: Acute Gastritis
- eliminate the cause
- prevent the cause in the future
- if vomiting - IV fluids, electrolytes, antiemetic (IV), NPO, bedrest, give vit B12, folic acid
- if severe - N/G, to lavage precipitating agent or suction
- Drug therapy: to reduce irritation of gastric mucosa - PPIs, H2R blockers, antiacids
- Relief of symptoms
Nursing Management of Chronic Gastritis
Eliminate cause - cessation of alcohol, abstinence from drugs, H.pylori eradications, combination of abx and antisecretory agent. for pernicious anemia - cobalamin tx
Lifestyle changes - non-irritating diet, 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 and pepsin
- pepsin is chief digesting enzyme in the stomach that breaks down proteins
Classification of Peptic Ulcers
and Based on what
Classified as:
- acute or chronic
Based on degree and duration of mucosal involvement
Location of PUD
Gastric and duodenal
PUD: Acute Ulcers
- Superficial erosion
- Minimal inflammation
- Or short duration
- Resolves quickly when cause is removed
PUD: Chronic Ulcers
- Long duration
- Erosion through muscular wall
- Formation of fibrous tissue
- Continually present for many months, or intermittently throughout lifetime
Causes of PUD
- many ulcers are caused by H.pylori infection or use of NSAIDS
PUD: Pathophysiology
- Stomach protected by gastric mucosal barrier
- Surface mucosa of stomach renewed q3 days
- Tissue injury caused by HCl leads to release of histamine -> vasodilation & increased capillary permeability -> histamine stimulates further secretion of acid and pepsin -> further mucosal erosion and destruction of blood vessels and bleeding -> ulceration
- with mucosal barrier disruption, comes increased blood flow. If blood flow insufficient, tissue injury occurs
Destructive Agents in PUD
H. pylori, ASA, NSAIDS, corticosteroids and some chemo meds
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 adults
- 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
Type 1 Gastric Ulcers
in the andrum, near lesser curvature
Type II
Combined gastric and duodenal
Type III
Prepyloric
Type IV
Ulcer in the proximal stomach and Cardia
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
Genetic etiology: persons with blood group O have increased incidence
H. pylori and duodenal ulcers
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
Clinical Manifestations PUD (5)
- Common for ps with PUD to have no pain or other symptoms
- When pain does occur:
with duodenal ulcer, “burning” or “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: Hemorrhage
- most common
- higher in duodenal ulcers than gastric ulcers
Complications of Chronic PUD: 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, should pain because of irritation to the phrenic nerve)
Complications of Chronic PUD: 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
Diagnostic Studies to confirm H.Pylori infection: non-invasive (4)
- serum/ whole blood antibody tests
- urea breath test
- barium studies
- lab tests (CBC, LFTs, FOB)
Diagnostic Studies to confirm H.Pylori infection: Invasive
- Biopsy of the stomach-rapid urease test
- Greater sensitivity and specificity than non-invasive methods but can’t be done without endoscopy
Collaborative care and Nursing Management of PUD: conservative therapy
Aim: decreasing degree of gastric acidity
- adequate rest
- medication therapy - adherence until completely healed important
- elimination of smoking
- nutrition 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 Peptic Ulcer Disease (6)
A vital part of therapy
Strict adherence is important
- histamine-2 receptor blockers (famotidine)
- proton pump inhibitors (pantoprazole)
- antibiotics (amoxicillin, clarithromycin)
- antacids ( aluminum carbonate)
- anticholinergics to decrease vagal stimulation of HCl secretion. Can also decrease gastric emptying so do not use in gastric ulcers if stasis of secretions increases discomfort.
- Cytoprotective drug therapy
Surgical Therapy for PUD
- uncommon
- treatment for complications or Gastric Ca
- Surgeries (partial gastrectomy, vagotomy - severing the vagus nerve)
Pyloroplasty - takes part of the stomach and putting it around the sphincter to tighten it
Complications of Surgery for PUD (3)
- Dumping syndrome: after a meal within 15-30 minutes, they will have vagal stimulation, weakness, and urge to defecate.
- Postprandial Hypoglycemia: low blood sugar that happens 1-3 hours after eating something with simple sugar. high insulin response to the glucose. limit carb intake
- Bile Reflux gastritis: bile that is released into SI washes back into the stomach and sometimes the esophagus - epigastric distress after meals and vomiting will alleviate it temporarily
Post-Op Care: Nutritional Therapy
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 I duration
