Patho Exam 2 Upper GI
Card Set Information
Patho Exam 2 Upper GI
Urinary, Endocrine, GI, Hepatobilary
What are the hostile aggressive factors in PUD?
What are the protective factors in PUD?
Blood flow to mucosa
Group of upper GI tract ulcerative disorders that develop whne GI tract is exposed to acid and pepsin secretions
What is the underlying problem in PUD?
Imbalance in aggressive and protective factors
- Increased gastric acidity (Oversecretion)
- Decreased prostaglandin production (NSAIDS)
- Interference with mucous layer (H. pylori infection)
What damages the mucosal layer?
Increased histamine secretion
Why is histamine released?
Released in response to damage done to organ wall
What does histamine release result in?
Increased pepsin and acid secretion (causing injury)
Local vasodilation (increasing capillary permeability- resulting in mucosal edema)
How does H. pylori survive?
Produces urea-splitting enzyme called urease, which breaks up urea into ammonia and bicarbonate forming a cloud
What diseases are attributed to H. pylori?
some Stomach cancers
What is the pathology behind H. pylori?
H. pylori secretes protease
Breaks through mucosal gel barrier
Triggers inflammatory response
Activation of inflammatory mediators
Resulting in: Inflammation-based Damage
What is the mechanism of injury for H. pylori?
What are the risk factors for NSAID-Induced PUD?
Advanced age r/t higher does longer
Higher doses of NSAIDS
Concomitant use of corticosteroids and anticoagulants (harm GI tract)
Serious systemic disorders (chronic comorbidities)
H. pylori infection
What is Cyclo-oxygenase (COX), that NSAIDS target?
Enzyme responsible for production of important biological mediators
What does COX 1 do (which NSAIDS inhibit)?
Protects the GI tract
produces gastric prostaglandins- PGE
therefore NSAIDS harm the GI tract inhibiting production of PGE
What does COX 2 do (which NSAIDS inhibit)?
Proinflammatory- causing pain
therefore NSAIDS inhibit pain and inflammation (why we take them)
What age group gets duodenal ulcers?
What age group gets Gastic ulcers and why?
Age 55 to 70
High doses of NSAIDS
Superficial damage to mucosa and submucosa layers
known as "stress ulcers"
Define Acute Ulcer
Penetration into muscle layer
if it eats through vascular- more bleeding
Define Perforating Ulcer
Approaching penetration of the wall
at this point- through the muscular and deep, it hurts
List the S&S of PUD
Asymptomatic until deeper
Weight loss r/t not eating from fear of inflammation
Bleeding (Hematemesis or melena)
Describe the pain associated with PUD
Burning, chewing pain
Located in the epigastric and back
Gastric- 1 to 2 hrs following meals
Duodenal- 2 to 4 hrs following meals
: antacids and sometimes eating (seen as a buffer)
What are the complications of PUD?
Perforation and Peritonitis
What are the causes of Hemorrhage r/t PUD?
Bleeding granulation tissue (which sweeps away granulation tissue which could heal the ulcer)
What are the causes of Obstruction r/t PUD?
Contraction of scar tissue
What does Obstruction r/t PUD do?
Can interfere with passage of GI contents (causing symptoms) (as the scar tissue develops it strinks causing smaller passageways)
What is Perforation r/t PUD?
Erosion through all layers of tract ex. GI contents through peritoneum causing peritonitis or can attach to other organs causing damage from gastric juices
List two types of Stress Ulcers and characteristics
painless upper GI bleed
Describe a Curling ulcer and cause
: physiologic stress- seen in critical care, top priority (must be corrected within 24 hours)
It is the shunting of blood
GI tissue becomes ischemia resulting in tissue acidosis
Describe Cushing ulcer and cause
: Increased intracranial pressure
More severe than curling ulcer
Compromised brain causes hypersecretion of gastric acid
Backflow (reflux) of gastric contents into esophagus
due to weakened or incompetent valve or physiological (feeding or NG tube)
List the sequence of events r/t GERD
Transient relaxation of esophagus
Reflux (from increased gastric volume and increased gastric/ abdominal pressure)
Esophageal mucosal exposure to gastric refluxate
Symptoms of GERD
What is the normal physiological response to reflux?
What is abnormal (GERD) response to reflux?
hyperemia (increased blood to organ)
What are the contributing factors to abnormal (GERD) response?
Increased exposure time
Highly acidic refluxate
What happens in Barrett's Esophagus (chronic GERD)?
Metaplasia condition- normal stratified squamous epithelium replaced by abnormal columnar epithelium
can result in esophageal cancer
List the clinical manifestations of Heartburn
: following meals and while lying down or bending over
Regurgitation of "sour" material
Atypical chest pain
Define acute gastritis
Transient gastric mucosal inflammation with the introduction of gastric irritants
List the 3 Major gastric irritants
Drugs or chemicals- common irritants (caffeine, NSAIDS, ETOH) and suppressed gastric PGE
Bacterial endotoxins (food poisoning)
H. pylori bacteria
List the Acute Gastritis Sequence of Events
Exposure to Gastric Irritant
Gastric inflammation caused by ETOH, Histamine, Metabolic disorders, and certain drugs
Focal or Generalized Erosion of surface epithelium (superficial)
List clinical manifestations of Acute Gastritis
Anorexia (from not wanting to eat from pain)
N/V (from pain in stomach)
Hematemesis (vomitting frank blood) and or melena (black tarry stool)
Describe Chronic Gastritis
Slow, progressive disorder (initally asymptomatic)
Begins with superficial inflammation
Gradually leads to destroyed functional cells
Stomach can atrophy and take on a diff appearance
What group is targeted with Chronic Gastritis?
What are the two types of Chronic Gastritis?
Type A (Atrophic Gastritis)- autoimmune
Type B (H. pylori)- slow destruction
Describe Chronic Gastritis: Type A (Atrophic)
Progressive Gastric Mucosa Degeneration from autoimmune disorder
What does Chronic gastritis type A reult in?
Loss of chief cells- decrease in pepsin (breakdown protein)
Loss of parietal cells- decreased HCL and intrensic factor (needed to absorb B12- resulting in pernicious anemia) and increase in Gastrin
List the characteristics of Chronic Gastritis: Type A
Disappearance of gastric folds (causing smooth pale non-functional stomach)
Visualization of submucosal blood vessels
Total or partial loss of mucosal lining
Describe Chronic Gastritis: Type B (H. pylori)
: Thinning and atrophy of mucosal layer
Resulting in decreased protection from autodigestive substances
List the clinical manifestations of Chronic Gastritis
Asymptomatic until advanced disease
Vague gastric distress
Pain from erosion
: sx of anemia, sx of vit B12 deficiency
Define Hiatal Hernia
Portion of upper stomach slips up or passes (herinates) through hiatus and into chest
Cause and potential contributing factors of Hiatal Hernia
: Larger than normal esophageal hiatus
Permanent shortening of esophagus
Abnormally loose attachment of esophagus to diaphragm
List the clinical manifestations of Hiatal Hernia
Worsens with certain activities (like lying down after eating)
How you treat H. pylori?
Combination therapy with 2 antibiotics for 2 weeks
How can you treat Upper GI disorders?
Increasing protective factors- antacids, sucralfate, Misoprostol
Decresing aggressive factors- Histamine 2 blockers, proton pump inhibitor, protectants, Cholingergic-Blockers
Why are antacids taken in combination?
The two drugs do the same thing, but balance out the others side effects
What are the major purposes of Antacids?
Reduce acid indigestion
Relief of Sx (heartburn, gastric distress)
Help protect mucosal layer
What is the MOA of large-dose Antacids?
Neutralizes acid through a chemical reaction in which the end product is water instead of acid
What is the MOA of small-dose Antacids?
Promote gastric mucosal defense mechanisms by increasing production of protective secretions (mucous and prostaglandins)
List the side effects of Antacids
Diarrhea or constipation
Rebound hypersensitivity (symptomatic when therapy stopped)
Chelation (binds to other drug to prevent absorption)
Altered stomach pH (other drug cannot break up)
Describe the antacid, Alginic acid and its MOA
Seaweed base makes it hydrophobic
Floats on top of chyme as a protectant when backflow present
What is the MOA of Sucralfate (Carafate)?
: alters when exposed to gastric acid, becomes sticky thick gel and adheres to ulcer crater as a protective barrier
Therefore is a mucosal protectant and promotes healing
List route, SE, and interactions of Sucralfate (Carafate)
PO- tablet or suspension
No major SE- works locally on active ulcer
Decreases other drugs absorption, take 2 hours apart
What is the MOA of Misoprostol (Cytotec)?
PGE replacement that is lost with NSAIDS (through stimulating COX 1)
Increases mucosal protective factors through being a synthetic PGE
State the therapeutic use of Misoprostol (Cytotec)
Approved for gastric ulcer secondary to NSAID therapy
List the side effects and contraindication of Misoprostol (Cytotec)
Contraindicated in Pregnancy (stimulates contractions)
What is gastric acid secretion stimulated by?
(body preparing acids for food)
What is the prototype Histamine type 2 receptor antagonists?
look for "-idine" endings
What is the MOA of cimetidine (Tagamet)?
Block H2 receptors
Reduces gastric acid secretions (blocks 90% of acids being formed)
List the SE and interactions for cimetidine (Tagamet)
: well tolerated
Slight increased risk for pneumonia in elderly (acids are in the stomach to fight bacteria, if chyme is aspirated without acids there is a risk for bacterial infection)
What is the final stage of gastric acid secretion?
H+ is a proton
If the pump is stopped then histamine and other acids are blocked from releasing
What is the prototype drug for Proton Pump Inhibitors?
look for "-prazole" suffix
What is the MOA of omeprazole (Prilosec)?
Blocks final production step
PPI binds to H+/K+ ATPase
Prevents release of HCl
highly effective (targets exiting cells, not entering)
List the SE and adverse effects of omeprazole (Prilosec)
Safe when taken short term
Slight increased risk for pnemonia when aspirated gastric contents by elderly resulting in bacterial infections
: Other PO drugs require acid pH to break down
List the nursing implications of omeprazole (Prilosec)
Limit use to 2 weeks- not permanent
Drug of choice when H2RA (Tagament) not effective
More expensive therefore insurance companies require proof of H2RA failure
Describe metoclopramide (Reglan) and its MOA
Prokinetic agent, antiemetic
: Stimulates gastric muscle contraction, and relaxation of pyloric and duodenal segments (helps peristalsis in the stomach)
Does not increase secretions
List the drug effects and SE of metoclopramide (Reglan)
: promotion of movement of substances through GI tract (temporarily move GI tract)
: many! Sedation or restlessness, Extrapyramidal reactions (involuntar limb, facial, or eye movements)
List the nursing implications of metoclopramide (Reglan)
Short term therapy
Check pt drug regimen therapy before initiating
Teach regaring possible side effects