Pathophysiology: Chapter 42: Alterations of Digestive Function

Question 1

Where in the brain is the vomiting center located?

a. Hypothalamus c. Pons
b. Medulla oblongata d. Midbrain

Answer 1

ANS: B
The vomiting center of the brain lies in the medulla oblongata. The other locations listed
are not related to vomiting.

Question 2

Antiemetic agents, such as domperidone and haloperidol, are antagonists for which
receptors?
a. 5-Hydroxytryptamine (5-HT) serotonin
b. Histamine-2
c. Acetylcholine
d. Dopamine

Answer 2

ANS: D
Metoclopramide, domperidone, and haloperidol are dopamine antagonists, making them
effective antiemetic agents. This selection is the only option that identifies a receptor that
is involved in the process of vomiting.

Question 3

What type of vomiting is caused by the direct stimulation of the vomiting center by
neurologic lesions involving the brainstem?
a. Retch c. Duodenal
b. Periodic d. Projectile

Answer 3

ANS: D
Of the available options, only projectile vomiting is caused by the direct stimulation of the
vomiting center by neurologic lesions, such as increased intracranial pressure, tumors, or
aneurysms involving the brainstem.

Question 4

Considering the normal frequency of bowel evacuation, how infrequently can evacuation
occur and still be considered within normal range?
a. Once a day
b. Once every 2 days
c. Once a week
d. Once every 2 weeks

Answer 4

ANS: C

Normal bowel habits range from two or three evacuations per day to one per week.

Question 5

How many stools per day are considered the upper limits of normal?

a. Two c. Five
b. Three d. Seven
l.

Answer 5

ANS: B

More than three stools per day is considered abnorma

Question 6

The adult intestine processes approximately how many liters of luminal content per day?

a. 3 c. 9
b. 6 d. 12

Answer 6

ANS: C
The adult intestine processes approximately 9 L of luminal content per day. Of this
amount, 2 L is ingested and the remaining 7 L consists of intestinal secretions.

Question 7

A person who has cholera would be expected to have which type of diarrhea?

a. Osmotic c. Small volume
b. Secretory d. Motility

Answer 7

ANS: B
Primary causes of secretory diarrhea are bacterial enterotoxins, particularly those released
by cholera or strains of Escherichia coli, and neoplasms, such as gastrinoma or thyroid
carcinoma. None of the other options are associated with secretory diarrhea.

Question 8

What type of diarrhea is a result of lactase deficiency?

a. Motility c. Secretory
b. Osmotic d. Small-volume

Answer 8

ANS: B
Malabsorption related to lactase deficiency, pancreatic enzyme or bile salt deficiency,
small intestine bacterial overgrowth, and celiac disease cause osmotic diarrhea. None of
the other options are associated with lactase deficiencies.

Question 9

Which statement is false concerning how abdominal pain is produced?
a. Chemical mediators, such as histamine, bradykinin, and serotonin, produce
abdominal pain.
b. Edema and vascular congestion produce abdominal pain by stretching.
c. Ischemia, caused by distention of bowel obstruction or mesenteric vessel
thrombosis, produces abdominal pain.
d. Low concentrations of anaerobes, such as Streptococci, Lactobacilli,
Staphylococci, Enterobacteria, and Bacteroides, produce abdominal pain.

Answer 9

ANS: D

Low concentrations of anaerobes are not typically a cause of abdominal pain.

Question 10

How can abdominal pain that is visceral in nature best be described?
a. Abdominal pain that is visceral in nature is diffused, vague, poorly localized, and
dull.
b. It travels from a specific organ to the spinal cord.
c. The pain lateralizes from only one side of the nervous system.
d. Abdominal pain is associated with the peristalsis of the gastrointestinal tract.

Answer 10

ANS: A
Pain is usually felt near the midline in the epigastrium (upper midabdomen), midabdomen,
or lower abdomen. The pain is poorly localized, is dull rather than sharp, and is difficult to
describe. None of the other options accurately describe this type of pain.

Question 11

What is the cause of gastroesophageal reflux disease?
a. Excessive production of hydrochloric acid
b. Zone of low pressure of the lower esophageal sphincter
c. Presence of Helicobacter pylori in the esophagus
d. Reverse muscular peristalsis of the esophagus
.

Answer 11

ANS: B
Normally, the resting tone of the lower esophageal sphincter maintains a zone of high
pressure that prevents gastroesophageal reflux. In individuals who develop reflux
esophagitis, this pressure tends to be lower than normal from either transient relaxation or
a weakness of the sphincter. This selection is the only option that accurately describes the
cause of gastroesophageal reflux disease

Question 12

What term is used to identify frank bleeding of the rectum?

a. Melena c. Occult bleeding
b. Hematochezia d. Hematemesis

Answer 12

ANS: B
Hematochezia is the only available option that is associated with frank bright red or
burgundy blood from the rectum.

Question 13

What is the cause of functional dysphagia?

a. Intrinsic mechanical obstruction
b. Extrinsic mechanical obstruction
c. Tumor
d. Neural or muscular disorders

Answer 13

ANS: D
Neural or muscular disorders that interfere with voluntary swallowing or peristalsis cause
functional dysphagia. This selection is the only option that accurately identifies a cause of
functional dysphagia.

Question 14

What is the cause of reflux esophagitis?

a. Immune response to gastroesophageal reflux
b. Delayed gastric emptying
c. Congenital anomaly
d. Secretory response to gastroesophageal reflux

Answer 14

ANS: B
Delayed gastric emptying contributes to reflux esophagitis by (1) lengthening the period
during which reflux is possible and (2) increasing the acid content of chyme. None of the
other options are accurate descriptions of the cause of reflux esophagitis.

Question 15

By what mechanism does intussusception cause an intestinal obstruction?
a. Telescoping of part of the intestine into another section of intestine, usually
causing strangulation of the blood supply
b. Twisting the intestine on its mesenteric pedicle, causing occlusion of the blood
supply
c. Loss of peristaltic motor activity in the intestine, causing an adynamic ileus
d. Forming fibrin and scar tissue that attach to the intestinal omentum, causing
obstruction

Answer 15

ANS: A
Intussusception is the telescoping of part of the intestine into another section of intestine,
usually causing strangulation of the blood supply. This selection is the only option that
accurately describes how intussusception causes an intestinal obstruction.

Question 16

What is the most immediate result of a small intestinal obstruction?

a. Vomiting c. Electrolyte imbalances
b. Dehydration d. Distention

Answer 16

ANS: D
Distention begins almost immediately, as gases and fluids accumulate proximal to the
obstruction. Within 24 hours, up to 8 L of fluid and electrolytes enters the lumen in the
form of saliva, gastric juice, bile, pancreatic juice, and intestinal secretions. Copious
vomiting or sequestration of fluids in the intestinal lumen prevents their reabsorption and
produces severe fluid and electrolyte disturbances.

Question 17

An intestinal obstruction at the pylorus or high in the small intestine causes metabolic
alkalosis by causing which outcome?
a. Gain of bicarbonate from pancreatic secretions that cannot be absorbed
b. Excessive loss of hydrogen ions normally absorbed from gastric juices
c. Excessive loss of potassium, promoting atony of the intestinal wall
d. Loss of bile acid secretions that cannot be absorbed

Answer 17

ANS: B
If the obstruction is at the pylorus or high in the small intestine, then metabolic alkalosis
initially develops as a result of excessive loss of hydrogen ions that normally would be
reabsorbed from the gastric juices. This selection is the only option that accurately
describes the cause of metabolic alkalosis in this situation.

Question 18

What are the cardinal symptoms of small intestinal obstruction?

a. Constant, dull pain in the lower abdomen relieved by defecation
b. Acute, intermittent pain 30 minutes to 2 hours after eating
c. Colicky pain caused by distention, followed by vomiting
d. Excruciating pain in the hypogastric area caused by ischemia

Answer 18

ANS: C
Of the options available, only colicky pain caused by distention followed by vomiting are
considered the cardinal symptoms of a small intestinal obstruction.

Question 19

What is a cause of chronic antral gastritis?

a. Helicobacter pylori bacteria
b. Development of autoantibodies to gastric H+/K+ ATPase
c. Pernicious anemia
d. Reflux of bile and alkaline pancreatic secretions

Answer 19

ANS: A
Chronic antral gastritis generally involves only the antrum and is more common than
fundal gastritis. It is caused by H. pylori bacteria or the chronic use of alcohol, tobacco,
and nonsteroidal antiinflammatory drugs. None of the other options are associated with the
cause of chronic antral gastritis.

Question 20

What is the primary cause of peptic ulcers?
a. Hypersecretion of gastric acid
b. Hyposecretion of pepsin
c. Helicobacter pylori
d. Escherichia coli
ANS: C
Infection with H. pylori is a primary cause of peptic ulcers.

Answer 20

ANS: C

Infection with H. pylori is a primary cause of peptic ulcers.

Question 21

A peptic ulcer may occur in all of the following areas except the:

a. Stomach c. Jejunum
b. Duodenum d. Esophagus

Answer 21

ANS: C
A peptic ulcer is a break, or ulceration, in the protective mucosal lining of the lower
esophagus, stomach, or duodenum. This type of ulcer is not associated with the jejunum.

Question 22

Which statement is false regarding the contributing factors of duodenal ulcers?
a. Bleeding from duodenal ulcers causes hematemesis or melena.
b. Gastric emptying is slowed, causing greater exposure of the mucosa to acid.
c. The characteristic pain begins 30 minutes to 2 hours after eating when the stomach
is empty.
d. Duodenal ulcers occur with greater frequency than other types of peptic ulcers.

Answer 22

ANS: B
Duodenal ulcers can be associated with altered mucosal defenses, rapid gastric emptying,
elevated serum gastrin levels, or acid production stimulated by smoking. The other options
provide correct information regarding duodenal ulcers

Question 23

After a partial gastrectomy or pyloroplasty, clinical manifestations that include increased
pulse, hypotension, weakness, pallor, sweating, and dizziness are the results of which
mechanism?
a. Anaphylactic reaction in which chemical mediators, such as histamine,
prostaglandins, and leukotrienes, relax vascular smooth muscles, causing shock
b. Postoperative hemorrhage during which a large volume of blood is lost, causing
hypotension with compensatory tachycardia
c. Concentrated bolus that moves from the stomach into the small intestine, causing
hyperglycemia and resulting in polyuria and eventually hypovolemic shock
d. Rapid gastric emptying and the creation of a high osmotic gradient in the small
intestine, causing a sudden shift of fluid from the blood vessels to the intestinal
lumen

Answer 23

ANS: D
Dumping syndrome occurs with varying severity in 5% to 10% of individuals who have
undergone partial gastrectomy or pyloroplasty. Rapid gastric emptying and the creation of
a high osmotic gradient in the small intestine cause a sudden shift of fluid from the
vascular compartment to the intestinal lumen. Plasma volume decreases, causing
vasomotor responses, such as increased pulse rate, hypotension, weakness, pallor,
sweating, and dizziness. Rapid distention of the intestine produces a feeling of epigastric
fullness, cramping, nausea, vomiting, and diarrhea. This selection is the only option that
accurately identifies the mechanism responsible for the described situation.

Question 24

Which statement is consistent with dumping syndrome?

a. Dumping syndrome usually responds well to dietary management.
b. It occurs 1 to 2 hours after eating.
c. Constipation is often a result of the dumping syndrome.
d. It can result in alkaline reflux gastritis.

Answer 24

ANS: A
Most individuals with the dumping syndrome respond well to dietary management. None
of the other options is associated with the dumping syndrome.

Question 25

What stimulates the desire to eat?

a. Agouti-related protein (AgRP)
b. Alpha-melanocyte–stimulating hormone (-MSH)
c. Cocaine- and amphetamine-regulated transcript (CART)
d. Peptide YY (PYY)

Answer 25

ANS: A
Specific neurons produce neuropeptide Y (NPY) and AgRP, which stimulates eating and
decreases metabolism (anabolic).

Question 26

Which structure regulates eating behavior and energy metabolism?

a. Anterior pituitary c. Posterior pituitary
b. Hypothalamus d. Parietal lobe

Answer 26

ANS: B
The arcuate nucleus (ARC) in the hypothalamus has two sets of neurons with opposing
effects that interact to regulate and balance food intake and energy metabolism. This
selection is the only option that regulates eating behavior and energy metabolism.

Question 27

Which symptom is characteristic of bulimia nervosa?

a. Recurrent episodes of binge eating with fears of not being able to stop eating.
b. Fear of becoming obese, despite progressive weight loss.
c. Perception that the body is fat when it is actually underweight.
d. Absence of three consecutive menstrual periods.

Answer 27

ANS: A
Diagnosis of bulimia is based on, among other findings, recurrent episodes of binge eating
during which the individual fears not being able to stop. The remaining options are
characteristic of anorexia nervosa.

Question 28

The most common clinical manifestation of portal hypertension is what type of bleeding?

a. Rectal c. Esophageal
b. Duodenal d. Intestinal

Answer 28

ANS: C
The vomiting of blood from bleeding esophageal varices is the most common clinical
manifestation of portal hypertension.

Question 29

What is the most common manifestation of portal hypertension–induced splenomegaly?

a. Leukopenia c. Erythrocytopenia
b. Thrombocytopenia d. Pancytopenia

Answer 29

ANS: B
Thrombocytopenia (decreased platelet count) is the most common manifestation of
congestive splenomegaly and can contribute to a tendency of increased bleeding.

Question 30

Which statement is false concerning the accumulation of fluid in the peritoneal cavity?
a. Impaired excretion of sodium by the kidneys promotes water retention.
b. Decreased oncotic pressure and increased hepatic sinusoidal hydrostatic pressure
cause the movement of fluid into the peritoneal cavity.
c. Decreased blood flow to the kidneys activates aldosterone, which retains sodium.
d. Circulating nitric oxide causes vasoconstriction, which forces fluid from the
capillaries into the peritoneal cavity.

Answer 30

ANS: D
The arterial vasodilation theory proposes that circulating nitric oxide or the release of
endotoxin from translocation of intestinal bacteria triggers arterial vasodilation of the
splanchnic organs early in the course of cirrhosis and stimulates renal sodium retention
through the renin-angiotensin-aldosterone system, increased sympathetic tone, and
changes in the intrarenal blood flow. The other options provide accurate information
regarding the accumulation of fluid in the peritoneal cavity.

Question 31

Which statement is false regarding the sources of increased ammonia that contribute to
hepatic encephalopathy?
a. End products of intestinal protein digestion are sources of increased ammonia.
b. Digested blood leaking from ruptured varices is a source of increased ammonia.
c. Accumulation of short-chain fatty acids that is attached to ammonia is a source of
increased ammonia.
d. Ammonia-forming bacteria in the colon are sources of increased ammonia.

Answer 31

ANS: C
The accumulation of short-chain fatty acids, serotonin, tryptophan, and false
neurotransmitters probably contributes to neural derangement and is not associated with
ammonia levels. The other options provide accurate information regarding how the
sources of ammonia contribute to hepatic encephalopathy.

Question 32

Hepatic fat accumulation is observed in which form of cirrhosis?

a. Biliary c. Postnecrotic
b. Metabolic d. Alcoholic

Answer 32

ANS: D
Alcoholic cirrhosis is a complex process that begins with fatty infiltration (hepatic
steatosis). Fat deposition (deposition of triglycerides) within the liver hepatocytes is
primarily caused by increased lipogenesis and decreased fatty acid oxidation by
hepatocytes. This selection is the only option that accurately identifies the correct form of
cirrhosis.

Question 33

Which statement is false concerning the pathophysiologic process of alcoholic cirrhosis?

a. Inflammation and damage leading to cirrhosis begin in the bile canaliculi.
b. Alcohol is transformed to acetaldehyde, which promotes liver fibrosis.
c. Mitochondrial function is impaired, decreasing oxidation of fatty acids.
d. Acetaldehyde inhibits export of proteins from the liver.

Answer 33

ANS: A
Biliary cirrhosis differs from alcoholic cirrhosis in that the damage and inflammation
leading to cirrhosis begin in bile canaliculi and bile ducts, rather than in the hepatocytes.
The other options provide true information regarding the pathophysiologic process of
alcoholic cirrhosis.

Question 34

Which statement is false regarding the pathophysiologic process of acute pancreatitis?
a. Bile duct or pancreatic duct obstruction blocks the outflow of pancreatic digestive
enzymes.
b. Acute pancreatitis can also result from direct cellular injury from drugs or viral
infection.
c. Acute pancreatitis is an autoimmune disease in which immunoglobulin G (IgG)
coats the pancreatic acinar cells; consequently, the pancreatic enzymes destroy the
cells.
d. Acute pancreatitis is usually mild and spontaneously resolves.

Answer 34

ANS: C
The backup of pancreatic secretions and the activation and release of enzymes (activated
trypsin activates chymotrypsin, lipase, and elastase) within the pancreatic acinar cells
cause acute pancreatitis, an obstructive disease. The activated enzymes cause
autodigestion (e.g., proteolysis, lipolysis) of the pancreatic cells and tissues, resulting in
inflammation. Acute pancreatitis is usually a mild disease and spontaneously resolves;
however, approximately 20% of those with the disease develop a severe acute pancreatitis
that requires hospitalization. Pancreatitis develops because of a blockage to the outflow of
pancreatic digestive enzymes caused by bile duct or pancreatic duct obstruction (e.g.,
gallstones). Acute pancreatitis can also result from direct cellular injury from drugs or
viral infection.

Question 35

The mutation of which gene is an early event associated with the pathogenetic origin of
esophageal cancer?
a. K-ras mutation c. myc
b. TP53 d. HER2

Answer 35

ANS: B
Mutation of the TP53 gene is an early event associated with esophageal cancer. This
selection is the only mutation from among the provided options.

Question 36

Obesity is defined as a body mass index (BMI) greater than what measurement?

a. 22 c. 28
b. 25 d. 30

Answer 36

ANS: D
Obesity is an energy imbalance, with caloric intake exceeding energy expenditure, and is
defined as a BMI greater than 30.