1
Q
Gastro-Esophageal Reflux Disease (GERD)
A
a syndrome, not a disease
the most prevalent acid-related disorder
2
Q
Cause of GERD
A
- 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)
3
Q
One of the primary factors in GERD
A
Incompetent lower esophageal sphincter (LES)
4
Q
How is GERD diagnosed
A
Diagnosis based on history and physical exam
5
Q
Clinical Manifestations of GERD (7)
A
- 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.
6
Q
Complications of GERD (3)
A
- Esophagitis
- Barretts esophagus
- Respiratory complications: bronchospams, laryngospasm, cricopharyngeal spasm
7
Q
Esophagitis
A
Scar tissue formation & decreased distensibility from repeated exposure
8
Q
Barretts esophagus
A
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
9
Q
Diagnostic Studies for GERD
A
Barium swallow studies
Endoscopy
Esophageal nanometric studies (measures the pressure in the esophagus and sphincter)
Radionuclide tests
10
Q
Collaborative Care GERD: Lifestyle Modification
A
- 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
11
Q
Collaborative Care GERD: Nutritional Therapy
A
- 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
12
Q
Collaborative Care GERD: Drug Therapy Goal
A
- Goals: improve LES function, increased esophageal clearance, decreased vol and acidity of reflux & protect esophageal mucosa
13
Q
Collaborative Care GERD: Drug Therapy - step-up approach vs step-down approach
A
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.
14
Q
Collaborative Care GERD: Drug therapy - cholinergic drugs
A
- increased LES pressure, increase esophageal emptying, and increase gastric emptying
15
Q
What is gastritis?
A
Inflammation of the gastric mucosa
16
Q
Categories of Gastritis
A
- acute or chronic
- diffuse or localized
17
Q
Subtypes of Chronic Gastritis
A
Autoimmune (involves the body and the funds of the stomach)
Diffuse Antral (affects primarily the antrum
Multifocal (diffse throughout the stomach
18
Q
Pathophysiology of Gastritis
A
- 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
19
Q
Causes of Gastritis: Drugs
A
- ASA, NSAIDS, corticosteroids, directly irritating and inhibit prostaglandin synthesis
20
Q
Causes of Gastritis: Dietary indiscretions
A
Alcoholic drinking binge - destruction of epithelial cells, mucosal congestion, edema, hemorrhage
A large quantities of spicy, irritating foods
21
Q
Causes of Gastritis: Microorganisms
A
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
22
Q
Clinical Manifestations of Acute Gastritis (7)
A
- 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
23
Q
Clinical Manifestations of Chronic Gastritis (3)
A
- 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
24
Q
Nursing Management: Acute Gastritis
A
- 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
25
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
26
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
27
Classification of Peptic Ulcers
and Based on what
Classified as:
- acute or chronic
Based on degree and duration of mucosal involvement
28
Location of PUD
Gastric and duodenal
29
PUD: Acute Ulcers
- Superficial erosion
- Minimal inflammation
- Or short duration
- Resolves quickly when cause is removed
30
PUD: Chronic Ulcers
- Long duration
- Erosion through muscular wall
- Formation of fibrous tissue
- Continually present for many months, or intermittently throughout lifetime
31
Causes of PUD
- many ulcers are caused by H.pylori infection or use of NSAIDS
32
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
33
Destructive Agents in PUD
H. pylori, ASA, NSAIDS, corticosteroids and some chemo meds
34
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
35
Type 1 Gastric Ulcers
in the andrum, near lesser curvature
36
Type II
Combined gastric and duodenal
37
Type III
Prepyloric
38
Type IV
Ulcer in the proximal stomach and Cardia
39
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
40
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
41
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
42
Complications of Chronic PUD: Hemorrhage
- most common
- higher in duodenal ulcers than gastric ulcers
43
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)
44
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
45
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)
46
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
47
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
48
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
49
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
50
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
51
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
NURS 412 Final Exam
flashcards
Decks in class (12)
# Cards
-
Liver Physiology17
-
Cirrhosis45
-
Cholelithiasis and Cholecystitis43
-
Disorders of the Pancreas37
-
Upper GI Problems51
-
Abnormal Vaginal Bleeding/Ectopic Pregnancy/Endometriosis26
-
Hysterectomy/Breast Cancer33
-
Renal and Urologic Problems44
-
Renal and Urologic Problems Cont'd32
-
Acute Kidney Injury53
-
Rhabdomyolysis6
-
Male Reproductive Disorders & Surgeries34
