Pathophysiology Exam 4 – Chapter 13 Study
Questions with Answers & Rationales
1) Understand the anatomy and physiology of the gastrointestinal tract.
2) What is gastritis? What causes acute gastritis? What are the signs/symptoms? What is
the typical course of the disease?
a) Gastritis inflammation of the stomach
b) Causes of acute gastritis
i) Taking too much NSAIDs and/or alcohol
ii) When stomach becomes too acidic
iii) Ingestion of bio and chem irritants
c) Signs/Symptoms
i) Nausea
ii) Vomiting
iii) Diarrhea
iv) May be associated with mucosal ulceration or bleeding
,d) Typical course of the disease
i) Self-limited inflammation of short duration
• Damage is minimal with rapid healing of the mucosa
ii) Resolves 5-10 days
,3) What causes chronic gastritis? What makes these substances irritating to the stomach?
What are the signs/symptoms? How is it treated?
a) Causes of chronic gastritis
i) H. pylori colonization in mucosa neutralizes stomach pH
ii) Recurring exposure to irritating substances
• Alcohol
• Aspirin
• NSAIDs
iii) Pernicious anemia Vit B12 deficient
b) Why are these substances irritating to the stomach?
i) NSAIDs aspirin, ibuprofen, naproxen, Advil, Aleve, etc.
• Inhibit cyclooxygenase (cox) enzyme
o COX-1: promotes synthesis of prostaglandin that protects gastric mucosa
▪ If taking them every day for something like that arthritis= problematic
o COX- 2: promotes synthesis of prostaglandins that mediate inflammation
blocks COX-1
▪ Drugs that selectively inhibit COX-2 increase risk for heart attack and
stroke
➢ Used to have 3 that were okay but then study showed risks
➢ Celebrex stayed while Vioxx and another were taken off the market
ii) Alcohol
• Stimulates gastric acid secretion more likely to irritate
• Fat soluble
• Passes through mucosa layer and is absorbed
iii) H. Pylori
• Small, curved, gram-neg organisms that colonize surface of gastric mucosa
• Grow within layer of mucus covering epithelial cells
• Produce urease that decomposes urea, a product of protein metabolism, into
ammonia
o Ammonia➔ neutralizes gastric acid allowing organisms to flourish; organisms
also produce enzymes that break down mucus layer
• Common infection that increases with age (50% by 50)
• Spreads via person-to-person through close contact and fecal-oral route
• Increased risk of gastric carcinoma intestinal metaplasia
• Increased risk of malignant lymphoma mucosa-associated lymphoid tissue/
MALT
c) Symptoms
i) Epigastric pain
ii) Indigestion
iii) Nausea
iv) Belching
v) Loss of appetite
vi) Bleeding can occur chronic
d) Treatment
i) Curing H. pylori infection with antibiotics often rapidly resolves the gastritis
ii) Eliminating irritants
• Alcohol cut down or stop drinking completely
• NSAIDs use another type of medication
iii) Antacids [ex. TUMS], Histamine (H-2) blockers [ex. zantec], PPIs, antiemeic
4) What are peptic ulcers? What causes them? What are the signs/symptoms? What are
possible complications? How are they treated?
, a) Sore or lesion in the mucous membrane
b) Cause
i) Digestion of mucosa due to increased acid secretions and digestive enzymes
gastric aid and pepsin (enzyme that breaks down food digestion)
ii) H. pylori injuries mucosa directly or through increased acid secretion by gastric
mucosa
iii) Common site distal stomach or proximal duodenum
c) Symptoms
i) Epigastric pain that varies from a gnawing, dull, aching, hunger-like pain to intestine
pain
• Eating or antacids usually relieves pain
ii) Heartburn
iii) Ingestion
iv) Anorexia
v) Nausea
vi) Vomiting
d) Possible complications
i) Hemorrhage if into a blood vessel
ii) Perforation leaking stomach fluid cavity, leading to peritonitis
iii) Obstruction from scarring
e) Treatment
i) H2 receptor blockers (Pepcid, Tagamet, zantac) or proton pump inhibitors/PPIs
(Prilosec, prevacid) to reduce gastric secretions
ii) Antacids to reduce gastric acidity
iii) Sucralfate [liquid] to coat and protect the mucosa
iv) If H. pylori is the cause, antibiotics (clarithromycin or azithomycin) combined with a
PPI and sucralfate
v) Any non-healing ulcers should be evaluated by endoscopy to rule out cancer
(especially gastric ulcers)
• Gastric ulcer and no results endoscopy and biopsy may be cancer
vi) Surgery in severe causes
5) What is acute enteritis? What causes it? What are the signs/symptoms? What is the
typical course of the disease?
a) Self-limiting, inflammation of bowel
b) Cause many different organisms and bacterial toxins
c) Symptoms
i) Nausea, vomiting
ii) Abdominal discomfort
iii) Loose stools
iv) In severe infections, bowel mucosa may be ulcerated and diarrheal stools may be
bloody
d) Course of disease short duration and may subside without specific treatment or may
respond to antibiotics or other agents
6) What are inflammatory bowel diseases? What causes them?
i) Inflammatory bowel diseases/ chronic enteritis Crohn’s disease and Ulcerative
colitis
b) Cause
i) Unknown
ii) Genetic predisposition
Questions with Answers & Rationales
1) Understand the anatomy and physiology of the gastrointestinal tract.
2) What is gastritis? What causes acute gastritis? What are the signs/symptoms? What is
the typical course of the disease?
a) Gastritis inflammation of the stomach
b) Causes of acute gastritis
i) Taking too much NSAIDs and/or alcohol
ii) When stomach becomes too acidic
iii) Ingestion of bio and chem irritants
c) Signs/Symptoms
i) Nausea
ii) Vomiting
iii) Diarrhea
iv) May be associated with mucosal ulceration or bleeding
,d) Typical course of the disease
i) Self-limited inflammation of short duration
• Damage is minimal with rapid healing of the mucosa
ii) Resolves 5-10 days
,3) What causes chronic gastritis? What makes these substances irritating to the stomach?
What are the signs/symptoms? How is it treated?
a) Causes of chronic gastritis
i) H. pylori colonization in mucosa neutralizes stomach pH
ii) Recurring exposure to irritating substances
• Alcohol
• Aspirin
• NSAIDs
iii) Pernicious anemia Vit B12 deficient
b) Why are these substances irritating to the stomach?
i) NSAIDs aspirin, ibuprofen, naproxen, Advil, Aleve, etc.
• Inhibit cyclooxygenase (cox) enzyme
o COX-1: promotes synthesis of prostaglandin that protects gastric mucosa
▪ If taking them every day for something like that arthritis= problematic
o COX- 2: promotes synthesis of prostaglandins that mediate inflammation
blocks COX-1
▪ Drugs that selectively inhibit COX-2 increase risk for heart attack and
stroke
➢ Used to have 3 that were okay but then study showed risks
➢ Celebrex stayed while Vioxx and another were taken off the market
ii) Alcohol
• Stimulates gastric acid secretion more likely to irritate
• Fat soluble
• Passes through mucosa layer and is absorbed
iii) H. Pylori
• Small, curved, gram-neg organisms that colonize surface of gastric mucosa
• Grow within layer of mucus covering epithelial cells
• Produce urease that decomposes urea, a product of protein metabolism, into
ammonia
o Ammonia➔ neutralizes gastric acid allowing organisms to flourish; organisms
also produce enzymes that break down mucus layer
• Common infection that increases with age (50% by 50)
• Spreads via person-to-person through close contact and fecal-oral route
• Increased risk of gastric carcinoma intestinal metaplasia
• Increased risk of malignant lymphoma mucosa-associated lymphoid tissue/
MALT
c) Symptoms
i) Epigastric pain
ii) Indigestion
iii) Nausea
iv) Belching
v) Loss of appetite
vi) Bleeding can occur chronic
d) Treatment
i) Curing H. pylori infection with antibiotics often rapidly resolves the gastritis
ii) Eliminating irritants
• Alcohol cut down or stop drinking completely
• NSAIDs use another type of medication
iii) Antacids [ex. TUMS], Histamine (H-2) blockers [ex. zantec], PPIs, antiemeic
4) What are peptic ulcers? What causes them? What are the signs/symptoms? What are
possible complications? How are they treated?
, a) Sore or lesion in the mucous membrane
b) Cause
i) Digestion of mucosa due to increased acid secretions and digestive enzymes
gastric aid and pepsin (enzyme that breaks down food digestion)
ii) H. pylori injuries mucosa directly or through increased acid secretion by gastric
mucosa
iii) Common site distal stomach or proximal duodenum
c) Symptoms
i) Epigastric pain that varies from a gnawing, dull, aching, hunger-like pain to intestine
pain
• Eating or antacids usually relieves pain
ii) Heartburn
iii) Ingestion
iv) Anorexia
v) Nausea
vi) Vomiting
d) Possible complications
i) Hemorrhage if into a blood vessel
ii) Perforation leaking stomach fluid cavity, leading to peritonitis
iii) Obstruction from scarring
e) Treatment
i) H2 receptor blockers (Pepcid, Tagamet, zantac) or proton pump inhibitors/PPIs
(Prilosec, prevacid) to reduce gastric secretions
ii) Antacids to reduce gastric acidity
iii) Sucralfate [liquid] to coat and protect the mucosa
iv) If H. pylori is the cause, antibiotics (clarithromycin or azithomycin) combined with a
PPI and sucralfate
v) Any non-healing ulcers should be evaluated by endoscopy to rule out cancer
(especially gastric ulcers)
• Gastric ulcer and no results endoscopy and biopsy may be cancer
vi) Surgery in severe causes
5) What is acute enteritis? What causes it? What are the signs/symptoms? What is the
typical course of the disease?
a) Self-limiting, inflammation of bowel
b) Cause many different organisms and bacterial toxins
c) Symptoms
i) Nausea, vomiting
ii) Abdominal discomfort
iii) Loose stools
iv) In severe infections, bowel mucosa may be ulcerated and diarrheal stools may be
bloody
d) Course of disease short duration and may subside without specific treatment or may
respond to antibiotics or other agents
6) What are inflammatory bowel diseases? What causes them?
i) Inflammatory bowel diseases/ chronic enteritis Crohn’s disease and Ulcerative
colitis
b) Cause
i) Unknown
ii) Genetic predisposition
