Actual Upper Gastro-Intestinal problems - Stomach, esophagus Flashcards
Gastro-Esophageal Reflux Disease (GERD)
Is a __syndrome_________; not a disease
Results when defenses of the lower esophagus are overwhelmed by reflux of stomach acidic contents into esophagus → results in irritation and inflammation
Cause is multi-factorial. One of the primary factors → incompetent lower esophageal sphincter (LES)
A common cause → hiatal hernia
-small opening in the diaphragm that the esophagus passes through. Stomach pushes up thru it into chest
-occurs when the upper part of the stomach pushes up into the chest through a small opening in the diaphragm
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Clinical manifestations:
-most common-heart burn________ (pyrosis)
-Burning, tight sensation, intermittently beneath lower sternum, radiating to throat and jaw
After ingestion of food that decreases LES pressure
-regurgitation
-Dysphagia
-Odynophagia (painful swallowing)
Complications of GERD:
(Related to direct exposure of gastric acid on esophageal mucosa)
- esophagitis: Scar tissue formation & ↓ distensibility from repeated exposure
- Barret’s esophagus: cells that normally present in small int and large int are in the esophagus (premalignant condition, increases risk for esophageal cancer). Will monitor q2-3 y w/ endoscope
- ## respiratory complications: bronchospasm, laryngospasm, cricopharyngeal spasm
Dx
Barium swallow studies
-swallow barium , xray, watch sphincter to see if it’s blocked or not
Endoscopy
Esophageal nanometric studies
- test pressure of LES
Radionuclide tests
Collaborative Care:
Nutritional therapy: AVOID
-Food can aggravate symptoms
Foods causing reflux:
Fatty foods (release cholecystokinin)
- Foods that lower LES pressure – chocolate, peppermint, caffeine
-Avoid milk at bedtime – increases gastric secretion
-Attention to diet & drugs that affect LES, acid secretion, or gastric emptying
Obese patients are encouraged to lose weight
Smokers are encouraged in smoking cessation
Drug therapy:
Goals: improve __LES_ function, ↑ esophageal clearance, ↓ vol and acidity of reflux, & protect esophageal mucosa
r 2 approaches to meds:
“step up”
-FIRST : try non-prescription meds like OTC histamine blockers or antacids
NEXT : H2Receptors - prescription
LASTLY: PPI – prescription
“step down”
-Start with PPI, end with antacid
Cholinergic drugs
- ↑ LES pressure, ↑esophageal emptying, ↑ gastric emptying
Disorders of the Stomach & Duodenum
Gastritis
Acute
Chronic
-autoimmune
-own immune system attacked
the cells ‘autoimu atrophic gastritis
-diffuse antral
- lower part of stomach that
connects to small int
-multifocal
-diffuses throughout the stomach
Causes:
1) Drugs
-ASA (aspirin),
NSAIDs (advil) - Blocks COX enzyme which blocks prostaglandins (prostaglandins- promotes tissue healing)
-corticosteroids___ : directly irritating and inhibit prostaglandin synthesis
2) Dietary indiscretions
-Alcoholic drinking binge – destruction of epithelial cells, mucosal congestion, edema, hemorrhage
-large quantities of spicy, irritating foods
3) 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 (ie Mycobacterium, CMV, Treponema pallidum)
Pathophysiology:
Result of breakdown in normal gastric mucosal barrier
Gastric mucosal barrier that protects stomach from acid. Acid is needed to breakdown food.
If barrier breaks down, = HCL diffuses into mucosa= inflammation -> ulcer
Clinical manifestations:
Acute gastritis
-N/V, a
-Epigastric tenderness
-Feeling of fullness
-hemorrhage__ with alcohol abuse
-vomiting/pooping black tar, hct/hgb
-Lasts a few hrs - few days
-Self–limiting- mucosa is expected to heal in a few days
Chronic Gastritis
-Some have no s/s
-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.
Nursing Management
ACUTE Gastritis
-Eliminate the cause
-Prevent the cause in the future
-If vomiting → tx IV fluids, electrolytes, antiemetic (IV), NPO, bedrest so don’t fall down
-if severe n/v -> ng lavage “stomach pumping”. Very unpleasant
Drug therapy – PPI, H2R blockers, antacids
to reduce irritation of gastric mucosa
Relief of symptoms
CHRONIC
Eliminate cause
Cessation of alcohol
Abstinence from drugs
H.pylori eradication → combination of abx and
antisecretory agent
For pernicious anemia- cobalamin tx. give vit B12, folic acid
Lifestyle changes:
-Non-irritating diet, in small meals
-smoking cessation
-Strict adherence to meds
-Adherence important -can lead to gastric cancer.
Peptic Ulcer Disease (PUD)
Acute
Chronic
mucosa
submucosa
muscle
serosa
normal, erosion, ulcer
Peptic Ulcer Disease (PUD)
Characterized by erosion of GI mucosa, resulting from digestive action of HCl and _pepsin_____.
Pepsin is the active enzyme in the stomach to break down proteins. Mucosal barrier protects from pepsin
Ulcer formation from pepsin
2 types. Based on: location, Degree, and duration of mucosal involvement
locations: Gastric (GU) and Duodenal (DU)
Acute
-goes down to submucosa, before muscle
Acute Ulcers
-Superficial erosion
-Minimal inflammation
-Of short duration
-Resolves quickly when cause is removed
Chronic
-goes down to muscle and serosa
-Risk of perforation – chronic because goes down to serosa
Chronic Ulcers
-Long duration
-Erosion through muscular wall
-Formation of fibrous tissue (scar)
-Continually present for many months, or intermittently throughout lifetime
patho:
-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
-less common but higher mortality than duodenal ulcers
-Most common sites: lesser curvature close to the antral junction.
-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
-smoking enhances
Duodenal Ulcers
-80% of all peptic ulcers.
-younger people
-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: PUD
Common to have no pain or other s/s
-When pain does occur with GU: high epigastric, __1-2 hrs after meals, “burning”, “gaseous”
-When pain does occur with DU: “burning”, “cramp-like”, mid-epigastric below xiphoid process
-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
Complications of Chronic PUD
-Most common: hemorrhage
duodenal ulcers > gastric ulcers
-pain in abd, blood tests, stool blood
most lethal: Perforation
-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
Gastric outlet obstruction (blockage)
-Increase in force needed to empty stomach → results in hypertrophy of stomach wall.
-A long history of ulcer pain.
-Involuntary vomiting, often projectile, common.
Dx of PUD
Endoscopy
Non-Invasive:
-Studies to confirm H. Pylori infection
-Serum/ whole blood antibody tests
-Urea breath test
-Barium studies
-Lab tests (CBC,LFTs, FOB)
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
PUD
Conservative therapy
Goal: ↓ degree of gastric acidity
-Adequate rest, bedrest
-Medication therapy- adherence until completely healed important
-Step up/step down meds + abx if H.Pylori
-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
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Drug therapy:
-A vital part of therapy!
Strict adherence is important.
Teach about adherence until completely healed & side effects
-Histamine-2 receptor (H2R) blockers. (ie. Famotidine)
-Proton pump inhibitors (ie. Pantoprazole)
-Antibiotics (ie. Amoxicillin, Clarithromycin)
-Antacids (ie. Aluminum carbonate)
-Anticholinergics (ie. Pirenzepine)
↓ vagal stimulation of HCl secretion
Do not use in gastric ulcers
Cytoprotective drug therapy (ie Misoprostol, Sucralfate)
Surgical Therapy for PUD
-sx uncommon
-mostly for complications or Gastric Ca
-Partial gastrectomy
Vagotomy: severing the vagus nerve
-Pyloroplasty: tightening sphincter
Complications of sx:
-Dumping Syndrome
-after a meal 25-30 min, feeling to defecate shortly after eating
-Postprandial Hypoglycemia
-low blood sugar 1-3 hours after eating something with simple sugar. Foods rapidly empty into small int= hypoglycemic
Tx – limit carb intake or take meds
-Bile Reflux Gastritis
-bile washes back into stomach
s/s epigastric distress after meals, vomiting to relieve temporarily
Post-op Care: PUD sx
-Stomach size reduced = eat smaller meals,
-no fluids with meals
-dry food
-low carb, 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
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