lOMoARcPSD|62982272
Week 5 GI
GERD
Pretest:
● Commonly associated with the loss of muscle tone at the lower esophageal sphincter (LES)
● Larger volumes of gastric contents generally increase gastric pressure, stimulating peristalsis and promoting a
faster rate of gastric emptying. Hypertonic solutions (and hypotonic), having a higher osmotic pressure than the
surrounding tissues, tend to delay gastric emptying.
● Obesity, smoking, and hiatal hernia = risk factors
Physiology of GI tract
● Mouth, esophagus, stomach, small intestine, large intestine, rectum, anus
● Responsible for breaking down ingested food, nutrient absorption, maintaining body water, eliminating waste
● Hormones and the autonomic nervous sys. regulate most digestive activities: hormone release, gastric motility,
substance for digestion
Physiology of Gastric Emptying
● Depending on volume, osmotic pressure, and chemical composition of gastric contents
● Longer to digest and break solids and fat == slower rate of emptying
Pathophysiology of GERD: backflow of acid or bile, caused by:
● Lower esophageal sphincter fn: decreased tone allows acid to regurg into the esophagus
● Esophageal motility: disrupted coordinated contraction causes delayed gastric emptying
● Delayed gastric emptying: causes esophagitis by extending the period during which reflux can occur and
increasing the acid content of chyme.
Clinical Manifestations: classic symptom = heartburn (pyrosis)
● Typical
○ Pyrosis: behind the sternum. HALLMARK
○ Regurgitation: sour or bitter taste
● Atypical
○ Chronic cough (irritation of the airway): persistent and not
always accompanied by heartburn
○ Asthma exacerbation (acid regurg into the airways):
triggers or worsens asthma
○ Laryngitis: inflammation of the voiced box
○ Sinusitis: irritation and inflammation of the sinuses
● Associated symptoms
○ Upper abd pain, especially within one hour of eating
○ Dysphagia: food sticking in the throat or hard to
swallowing
○ Belching and flatulence
○ Sleep disturbances
○ Worsening of s/s in supine, esp. after meals
Risk factors: obesity, smoking, hiatal hernia
● Obesity: slows gastric emptying == prolonged retention of food in the stomach and risk of reflux
● Smoking: weakens the lower esophageal sphincter Fn
● Hiatal hernia: a structural risk factor. The stomach protrudes through the diaphragmatic opening, impacting
sphincter == less effective in preventing the backflow of stomach contents into the esophagus
Dx and Tx
● Dx: based on hx and clinical manifestations.
● Tx:
1
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
○ Initially includes PPI (1st thing in the morning) and lifestyle changes (diet, weight loss, smoking cessation,
elevating the HOB, avoid tight clothing) == 6 weeks
○ If no change with PPI and lifestyle change in 6 weeks == esophageal endoscopy to confirm a dx or rule out
other conditions (can show esophagitis, gastric ulcers, presence of hiatal hernia, esophageal strictures).
Impedance/pH monitoring can measure acidity and mvt of stomach contents into esophagus. Fundoplication
= most common surgical intervention if medical tx fails.
○ Persistent esophagitis suggests that the inflammation of the esophagus has not responded adequately to the
prescribed interventions. The client continuing to have symptoms may be due to the development of
esophageal strictures, which can hinder the passage of food and contribute to ongoing discomfort. If gastric
ulcers are detected, it could explain ongoing symptoms and suggest that acid suppression therapy might not
be effectively controlling acid production. Identification of a hiatal hernia may contribute to ongoing
symptoms, as it can facilitate the reflux of stomach contents into the esophagus.
○ Diet: see below + oatmeal, broccoli, salad of non-acidic veggies and lean proteins, brown rice, lean proteins
(chicken etc.) are low in fact. Avoid carbonated drinks.
2
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
Obstructive GI Disorders: esophageal stricture, appendicitis
Pretest:
● Esophageal stricture: mainly caused by chronic inflammation and the development of scar tissue
● The most common cause of appendicitis is the obstruction of the appendix by a fecalith (hardened stool), leading
to a buildup of bacteria, inflammation, and ultimately appendicitis.
Physiology of GI system:
● Ingestion: intake
● Secretion: release of digestive juices and enzymes to break down food
● Propulsion: peristalsis
● Digestion: mechanical (breakdown into small pieces) and chemical (enzymes)
● Absorption: primarily in the small intestine. Animo acids, fatty acids, glucose, and minerals = into blood
● Transport: through the bloodstream to cells and tissues
● Storage and metabolism: stored in the liver and adipose tissue.
● Formation of feces: waste stored in the rectum until defecation
● Regulation: hormones (gastrin, secretin, cholecystokinin) and nerve signals regulate the digestive process.
Patho of esophageal stricture: narrowing of the esophagus leading to dysphagia and other s/s. The patho involves the
development of scar tissue or other structural changes resulting in a reduced diameter of the esophagus.
● Swallowing: coordinated contraction
● Peristalsis: involuntary contraction and relaxation of muscles to propel food into the stomach
● Lower esophageal sphincter (LES): Contracted to prevent reflux. If not functioning well == GERD
Esophageal stricture risk factors:
● GERD: backflow == inflammation and irritation == formation of scar tissue == narrowing the esophagus
● Esophagitis: inflammation caused by infection, meds, autoimmune
● Ingestion of caustic substances: swallowing of strong acids or bases == scar tissue from healing process
● Radiation therapy: radiation-induced scar tissue
● Spicy food and family hx of stricture are not direct risk factors
Esophageal stricture: Clinical manifestations, Dx, Tx:
● Manifestations: dysphagia, sensation of food sticking, pain or discomfort during swallowing
● Dx: hx, physical, imaging (barium swallow or endoscopy)
● Tx: meds to reduce inflammation (PPI etc.), dilation of the stricture (with a balloon or dilators during endo), tx
underlying disease. If severe, surgical intervention.
Patho of Appendicitis: Medical ER, requires surgical removal
● Obstruction by feces, foreign bodies, or swollen lymphoid tissue.
● Leading to a buildup of mucus, bacteria, and other debris within the appendix
● Causing inflammation and increased pressure
● Resulting in the appendix being inflamed, swollen, and filled with pus.
● The increased pressure within the inflamed appendix can compromise blood flow, leading to ischemia and
necrosis.
● Eventually leads to perforation, peritonitis, and the formation of an abscess.
Appendicitis Risk Factors and Manifestations:
● Occurs at any age, most commonly 10-19 yo. Family hx increases the risk
● Manifestations:
○ Abd pain: HALLMARK, pain initially around the umbilicus, later to RLQ, dull, vague discomfort, then
progressing to sharp, intense pain.
○ N/V: common symptoms, often occurring after the onset of abd pain
○ Loss of appetite
○ Fever: low-grade fever d/t inflammation
○ Rebound tenderness: increases when pressure is released in RLQ
○ Guarding: involuntary muscle contractions and guarding in response to pain
○ Peritonitis: after rupture, leading to intense abd pain, tenderness, fever, and abd rigidity
Appendicitis Dx:
3
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
● Hx: onset, nature of symptoms, focus on location, progression, associated s/s, alleviating or worsening factors
● Physical: palpating should be delayed after other assessments. Assess rebound tenderness in addition to:
○ Rovsing’s sign: palpate LLQ, if pressure here causes pain at McBurney’s point on the R side, it is + for dx
○ McBurney’s point: R side approx ⅓ from the anterior superior to the umbilicus. If pain, +
● Lab: CBC (elevated, but not specific to appendicitis), UA (rule out UTI), HCG (rule out ectopic pregnancy), CRP
(elevated if inflammation)
● Imaging: CT (most common), US
Appendicitis Tx: Appendectomy to prevent rupture, peritonitis, or abscess. Laparoscopic or open
● Pre-op: give abx. if abscess, drain before appendectomy, can also give IV pain meds and fluid, NPO
● Post-op: monitor for complications, pain meds, and gradual PO intake.
● Resume normal activities within a few weeks.
A history of GERD and long-term untreated esophagitis can lead to chronic inflammation and fibrosis of the esophagus,
increasing the risk of esophageal stricture development.
While difficulty swallowing may be a symptom of esophageal stricture, a recent diagnosis of IBS is not directly associated
with an increased risk of esophageal stricture.
Regular use of NSAIDs may contribute to gastrointestinal issues, but it is not a primary risk factor for esophageal stricture.
A family history of esophageal cancer is a concern, but occasional heartburn alone is not a significant risk factor for
esophageal stricture.
Occasional choking on food may indicate a risk of aspiration but is not a strong predictor of esophageal stricture. Rapid
eating can contribute to this symptom but is not a primary risk factor for stricture development.
4
Downloaded by elizabeth moses ()
Week 5 GI
GERD
Pretest:
● Commonly associated with the loss of muscle tone at the lower esophageal sphincter (LES)
● Larger volumes of gastric contents generally increase gastric pressure, stimulating peristalsis and promoting a
faster rate of gastric emptying. Hypertonic solutions (and hypotonic), having a higher osmotic pressure than the
surrounding tissues, tend to delay gastric emptying.
● Obesity, smoking, and hiatal hernia = risk factors
Physiology of GI tract
● Mouth, esophagus, stomach, small intestine, large intestine, rectum, anus
● Responsible for breaking down ingested food, nutrient absorption, maintaining body water, eliminating waste
● Hormones and the autonomic nervous sys. regulate most digestive activities: hormone release, gastric motility,
substance for digestion
Physiology of Gastric Emptying
● Depending on volume, osmotic pressure, and chemical composition of gastric contents
● Longer to digest and break solids and fat == slower rate of emptying
Pathophysiology of GERD: backflow of acid or bile, caused by:
● Lower esophageal sphincter fn: decreased tone allows acid to regurg into the esophagus
● Esophageal motility: disrupted coordinated contraction causes delayed gastric emptying
● Delayed gastric emptying: causes esophagitis by extending the period during which reflux can occur and
increasing the acid content of chyme.
Clinical Manifestations: classic symptom = heartburn (pyrosis)
● Typical
○ Pyrosis: behind the sternum. HALLMARK
○ Regurgitation: sour or bitter taste
● Atypical
○ Chronic cough (irritation of the airway): persistent and not
always accompanied by heartburn
○ Asthma exacerbation (acid regurg into the airways):
triggers or worsens asthma
○ Laryngitis: inflammation of the voiced box
○ Sinusitis: irritation and inflammation of the sinuses
● Associated symptoms
○ Upper abd pain, especially within one hour of eating
○ Dysphagia: food sticking in the throat or hard to
swallowing
○ Belching and flatulence
○ Sleep disturbances
○ Worsening of s/s in supine, esp. after meals
Risk factors: obesity, smoking, hiatal hernia
● Obesity: slows gastric emptying == prolonged retention of food in the stomach and risk of reflux
● Smoking: weakens the lower esophageal sphincter Fn
● Hiatal hernia: a structural risk factor. The stomach protrudes through the diaphragmatic opening, impacting
sphincter == less effective in preventing the backflow of stomach contents into the esophagus
Dx and Tx
● Dx: based on hx and clinical manifestations.
● Tx:
1
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
○ Initially includes PPI (1st thing in the morning) and lifestyle changes (diet, weight loss, smoking cessation,
elevating the HOB, avoid tight clothing) == 6 weeks
○ If no change with PPI and lifestyle change in 6 weeks == esophageal endoscopy to confirm a dx or rule out
other conditions (can show esophagitis, gastric ulcers, presence of hiatal hernia, esophageal strictures).
Impedance/pH monitoring can measure acidity and mvt of stomach contents into esophagus. Fundoplication
= most common surgical intervention if medical tx fails.
○ Persistent esophagitis suggests that the inflammation of the esophagus has not responded adequately to the
prescribed interventions. The client continuing to have symptoms may be due to the development of
esophageal strictures, which can hinder the passage of food and contribute to ongoing discomfort. If gastric
ulcers are detected, it could explain ongoing symptoms and suggest that acid suppression therapy might not
be effectively controlling acid production. Identification of a hiatal hernia may contribute to ongoing
symptoms, as it can facilitate the reflux of stomach contents into the esophagus.
○ Diet: see below + oatmeal, broccoli, salad of non-acidic veggies and lean proteins, brown rice, lean proteins
(chicken etc.) are low in fact. Avoid carbonated drinks.
2
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
Obstructive GI Disorders: esophageal stricture, appendicitis
Pretest:
● Esophageal stricture: mainly caused by chronic inflammation and the development of scar tissue
● The most common cause of appendicitis is the obstruction of the appendix by a fecalith (hardened stool), leading
to a buildup of bacteria, inflammation, and ultimately appendicitis.
Physiology of GI system:
● Ingestion: intake
● Secretion: release of digestive juices and enzymes to break down food
● Propulsion: peristalsis
● Digestion: mechanical (breakdown into small pieces) and chemical (enzymes)
● Absorption: primarily in the small intestine. Animo acids, fatty acids, glucose, and minerals = into blood
● Transport: through the bloodstream to cells and tissues
● Storage and metabolism: stored in the liver and adipose tissue.
● Formation of feces: waste stored in the rectum until defecation
● Regulation: hormones (gastrin, secretin, cholecystokinin) and nerve signals regulate the digestive process.
Patho of esophageal stricture: narrowing of the esophagus leading to dysphagia and other s/s. The patho involves the
development of scar tissue or other structural changes resulting in a reduced diameter of the esophagus.
● Swallowing: coordinated contraction
● Peristalsis: involuntary contraction and relaxation of muscles to propel food into the stomach
● Lower esophageal sphincter (LES): Contracted to prevent reflux. If not functioning well == GERD
Esophageal stricture risk factors:
● GERD: backflow == inflammation and irritation == formation of scar tissue == narrowing the esophagus
● Esophagitis: inflammation caused by infection, meds, autoimmune
● Ingestion of caustic substances: swallowing of strong acids or bases == scar tissue from healing process
● Radiation therapy: radiation-induced scar tissue
● Spicy food and family hx of stricture are not direct risk factors
Esophageal stricture: Clinical manifestations, Dx, Tx:
● Manifestations: dysphagia, sensation of food sticking, pain or discomfort during swallowing
● Dx: hx, physical, imaging (barium swallow or endoscopy)
● Tx: meds to reduce inflammation (PPI etc.), dilation of the stricture (with a balloon or dilators during endo), tx
underlying disease. If severe, surgical intervention.
Patho of Appendicitis: Medical ER, requires surgical removal
● Obstruction by feces, foreign bodies, or swollen lymphoid tissue.
● Leading to a buildup of mucus, bacteria, and other debris within the appendix
● Causing inflammation and increased pressure
● Resulting in the appendix being inflamed, swollen, and filled with pus.
● The increased pressure within the inflamed appendix can compromise blood flow, leading to ischemia and
necrosis.
● Eventually leads to perforation, peritonitis, and the formation of an abscess.
Appendicitis Risk Factors and Manifestations:
● Occurs at any age, most commonly 10-19 yo. Family hx increases the risk
● Manifestations:
○ Abd pain: HALLMARK, pain initially around the umbilicus, later to RLQ, dull, vague discomfort, then
progressing to sharp, intense pain.
○ N/V: common symptoms, often occurring after the onset of abd pain
○ Loss of appetite
○ Fever: low-grade fever d/t inflammation
○ Rebound tenderness: increases when pressure is released in RLQ
○ Guarding: involuntary muscle contractions and guarding in response to pain
○ Peritonitis: after rupture, leading to intense abd pain, tenderness, fever, and abd rigidity
Appendicitis Dx:
3
Downloaded by elizabeth moses ()
, lOMoARcPSD|62982272
● Hx: onset, nature of symptoms, focus on location, progression, associated s/s, alleviating or worsening factors
● Physical: palpating should be delayed after other assessments. Assess rebound tenderness in addition to:
○ Rovsing’s sign: palpate LLQ, if pressure here causes pain at McBurney’s point on the R side, it is + for dx
○ McBurney’s point: R side approx ⅓ from the anterior superior to the umbilicus. If pain, +
● Lab: CBC (elevated, but not specific to appendicitis), UA (rule out UTI), HCG (rule out ectopic pregnancy), CRP
(elevated if inflammation)
● Imaging: CT (most common), US
Appendicitis Tx: Appendectomy to prevent rupture, peritonitis, or abscess. Laparoscopic or open
● Pre-op: give abx. if abscess, drain before appendectomy, can also give IV pain meds and fluid, NPO
● Post-op: monitor for complications, pain meds, and gradual PO intake.
● Resume normal activities within a few weeks.
A history of GERD and long-term untreated esophagitis can lead to chronic inflammation and fibrosis of the esophagus,
increasing the risk of esophageal stricture development.
While difficulty swallowing may be a symptom of esophageal stricture, a recent diagnosis of IBS is not directly associated
with an increased risk of esophageal stricture.
Regular use of NSAIDs may contribute to gastrointestinal issues, but it is not a primary risk factor for esophageal stricture.
A family history of esophageal cancer is a concern, but occasional heartburn alone is not a significant risk factor for
esophageal stricture.
Occasional choking on food may indicate a risk of aspiration but is not a strong predictor of esophageal stricture. Rapid
eating can contribute to this symptom but is not a primary risk factor for stricture development.
4
Downloaded by elizabeth moses ()
