NURS 231/NURS231 Module 10 V2 |
Pathophysiology Q&A with Rationale | Portage
Learning
1. Which of the following describes the primary pathophysiology of Achalasia?
A. Dilation of the esophageal veins due to portal hypertension
B. Erosion of the esophageal lining due to gastric acid
C. Incomplete relaxation of the lower esophageal sphincter (LES)
D. Protrusion of the stomach through the diaphragm
Correct Answer: C
Explanation: Achalasia is a motility disorder where the lower esophageal sphincter fails to
relax properly during swallowing. This is typically caused by a loss of inhibitory neurons in
the myenteric plexus. Consequently, food becomes trapped in the esophagus, leading to
progressive dysphagia and esophageal dilation.
2. A patient with Gastroesophageal Reflux Disease (GERD) is at increased risk for which
cellular change in the esophagus?
A. Squamous cell hyperplasia
B. Coagulative necrosis
C. Barrett esophagus (metaplasia)
D. Atrophy of the mucosal lining
,Correct Answer: C
Explanation: Chronic exposure to stomach acid in GERD can cause the normal squamous
epithelium of the esophagus to be replaced by columnar epithelium. This process is known
as Barrett esophagus, which is a form of metaplasia. This condition is clinically significant
because it increases the risk of developing esophageal adenocarcinoma.
3. Which factor is most commonly associated with the development of Peptic Ulcer Disease
(PUD)?
A. High dietary fiber intake
B. Excessive intake of alkaline foods
C. Chronic use of acetaminophen
D. Helicobacter pylori infection
Correct Answer: D
Explanation: Helicobacter pylori is a gram-negative bacterium that colonizes the gastric
mucosa and is the leading cause of peptic ulcers. It produces urease and toxins that
provoke a chronic inflammatory response, weakening the protective mucous barrier.
Eradication of the infection is essential for permanent healing of the ulcer.
4. Which clinical manifestation is a hallmark of Crohn’s disease but not typically seen in
Ulcerative Colitis?
A. Continuous involvement of the colon
B. Bloody diarrhea with mucus
, C. Skip lesions throughout the GI tract
D. Inflammation limited to the mucosal layer
Correct Answer: C
Explanation: Crohn’s disease is characterized by skip lesions, which are areas of
inflammation separated by healthy tissue. Unlike Ulcerative Colitis, which affects the colon
continuously starting from the rectum, Crohn’s can affect any part of the digestive tract. It
also involves transmural inflammation, which often leads to fistulas and strictures.
5. What is the primary cause of ascites in patients with liver cirrhosis?
A. Increased oncotic pressure and decreased portal pressure
B. Excessive production of bile salts
C. Portal hypertension and decreased albumin synthesis
D. Increased systemic blood pressure
Correct Answer: C
Explanation: Ascites develops in cirrhosis due to a combination of portal hypertension and
hypoalbuminemia. Increased pressure in the portal vein forces fluid into the peritoneal
cavity, while low albumin levels reduce the oncotic pressure necessary to keep fluid in the
vessels. This leads to the characteristic abdominal distension seen in advanced liver
disease.
Pathophysiology Q&A with Rationale | Portage
Learning
1. Which of the following describes the primary pathophysiology of Achalasia?
A. Dilation of the esophageal veins due to portal hypertension
B. Erosion of the esophageal lining due to gastric acid
C. Incomplete relaxation of the lower esophageal sphincter (LES)
D. Protrusion of the stomach through the diaphragm
Correct Answer: C
Explanation: Achalasia is a motility disorder where the lower esophageal sphincter fails to
relax properly during swallowing. This is typically caused by a loss of inhibitory neurons in
the myenteric plexus. Consequently, food becomes trapped in the esophagus, leading to
progressive dysphagia and esophageal dilation.
2. A patient with Gastroesophageal Reflux Disease (GERD) is at increased risk for which
cellular change in the esophagus?
A. Squamous cell hyperplasia
B. Coagulative necrosis
C. Barrett esophagus (metaplasia)
D. Atrophy of the mucosal lining
,Correct Answer: C
Explanation: Chronic exposure to stomach acid in GERD can cause the normal squamous
epithelium of the esophagus to be replaced by columnar epithelium. This process is known
as Barrett esophagus, which is a form of metaplasia. This condition is clinically significant
because it increases the risk of developing esophageal adenocarcinoma.
3. Which factor is most commonly associated with the development of Peptic Ulcer Disease
(PUD)?
A. High dietary fiber intake
B. Excessive intake of alkaline foods
C. Chronic use of acetaminophen
D. Helicobacter pylori infection
Correct Answer: D
Explanation: Helicobacter pylori is a gram-negative bacterium that colonizes the gastric
mucosa and is the leading cause of peptic ulcers. It produces urease and toxins that
provoke a chronic inflammatory response, weakening the protective mucous barrier.
Eradication of the infection is essential for permanent healing of the ulcer.
4. Which clinical manifestation is a hallmark of Crohn’s disease but not typically seen in
Ulcerative Colitis?
A. Continuous involvement of the colon
B. Bloody diarrhea with mucus
, C. Skip lesions throughout the GI tract
D. Inflammation limited to the mucosal layer
Correct Answer: C
Explanation: Crohn’s disease is characterized by skip lesions, which are areas of
inflammation separated by healthy tissue. Unlike Ulcerative Colitis, which affects the colon
continuously starting from the rectum, Crohn’s can affect any part of the digestive tract. It
also involves transmural inflammation, which often leads to fistulas and strictures.
5. What is the primary cause of ascites in patients with liver cirrhosis?
A. Increased oncotic pressure and decreased portal pressure
B. Excessive production of bile salts
C. Portal hypertension and decreased albumin synthesis
D. Increased systemic blood pressure
Correct Answer: C
Explanation: Ascites develops in cirrhosis due to a combination of portal hypertension and
hypoalbuminemia. Increased pressure in the portal vein forces fluid into the peritoneal
cavity, while low albumin levels reduce the oncotic pressure necessary to keep fluid in the
vessels. This leads to the characteristic abdominal distension seen in advanced liver
disease.
