Chapter 41: Alterations of Digestive Function

MULTIPLE CHOICE
1. Where in the brain is the vomiting center located?
a. Hypothalamus
c. Pons
b. Medulla oblongata
d. Midbrain
ANS: B

The vomiting center of the brain lies in the medulla oblongata. The other locations listed are
not related to vomiting.
PTS: 1

REF: Page 1424

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
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.
PTS: 1

REF: Page 1424

3. What type of vomiting is caused by the direct stimulation of the vomiting center by neurologic

lesions involving the brainstem?

a. Retch
b. Periodic

c. Duodenal
d. Projectile

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.
PTS: 1

REF: Page 1424

4. Considering the normal frequency of bowel evacuation, how infrequently can evacuation

occur and still be considered within normal range?

c. Once a week
d. Once every 2 weeks

a. Once a day
b. Once every 2 days
ANS: C

Normal bowel habits range from two or three evacuations per day to one per week.
PTS: 1

REF: Page 1428

5. How many stools per day are considered the upper limits of normal?
a. Two
c. Five

b. Three

d. Seven

ANS: B

More than three stools per day is considered abnormal.

PTS: 1

REF: Page 1428

6. The adult intestine processes approximately how many liters of luminal content per day?
a. 3
c. 9
b. 6
d. 12
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.
PTS: 1

REF: Page 1425

7. A person who has cholera would be expected to have which type of diarrhea?
a. Osmotic
c. Small volume
b. Secretory
d. Motility
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.
PTS: 1

REF: Page 1425

8. What type of diarrhea is a result of lactase deficiency?

a. Motility
c. Secretory
b. Osmotic
d. Small-volume
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.
PTS: 1

REF: Page 1425

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.

ANS: D

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

PTS: 1

REF: Page 1426

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.
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.
PTS: 1

REF: Page 1426

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
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.
PTS: 1

REF: Page 1429

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

a. Melena
c. Occult bleeding
b. Hematochezia
d. Hematemesis
ANS: B

Hematochezia is the only available option that is associated with frank bright red or burgundy
blood from the rectum.
PTS: 1

REF: Page 1428

13. What is the cause of functional dysphagia?

a. Intrinsic mechanical obstruction
c. Tumor
b. Extrinsic mechanical obstruction
d. Neural or muscular disorders
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.
PTS: 1

REF: Page 1428

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
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.
PTS: 1

REF: Page 1429

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
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.
PTS: 1

REF: Page 1431 | Table 41-2

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

a. Vomiting
c. Electrolyte imbalances
b. Dehydration
d. Distention
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.
PTS: 1

REF: Pages 1431-1432

17. An intestinal obstruction at the pylorus or high in the small intestine causes metabolic

alkalosis by causing which outcome?

Gain of bicarbonate from pancreatic secretions that cannot be absorbed
Excessive loss of hydrogen ions normally absorbed from gastric juices
Excessive loss of potassium, promoting atony of the intestinal wall
Loss of bile acid secretions that cannot be absorbed

a.
b.
c.
d.

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.

PTS: 1

REF: Page 1432

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
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.
PTS: 1

REF: Pages 1432-1433

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
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.
PTS: 1

REF: Page 1435

20. What is the primary cause of peptic ulcers?

a. Hypersecretion of gastric acid
c. Helicobacter pylori
b. Hyposecretion of pepsin
d. Escherichia coli
ANS: C

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

PTS: 1

REF: Page 1435

21. A peptic ulcer may occur in all of the following areas except the:
a. Stomach
c. Jejunum
b. Duodenum
d. Esophagus
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.
PTS: 1

REF: Page 1435

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.
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.
PTS: 1

REF: Page 1435

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
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.
PTS: 1

REF: Page 1440

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.
ANS: A

Most individuals with the dumping syndrome respond well to dietary management. None of
the other options is associated with the dumping syndrome.
PTS: 1

REF: Page 1440

25. What stimulates the desire to eat?

a. Agouti-related protein (AgRP)
b. Alpha-melanocytestimulating hormone (-MSH)
c. Cocaine- and amphetamine-regulated transcript (CART)

d. Peptide YY (PYY)
ANS: A

Specific neurons produce neuropeptide Y (NPY) and AgRP, which stimulates eating and
decreases metabolism (anabolic).
PTS: 1

REF: Page 1448

26. Which structure regulates eating behavior and energy metabolism?

a. Anterior pituitary
c. Posterior pituitary
b. Hypothalamus
d. Parietal lobe
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.
PTS: 1

REF: Pages 1447-1448

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.
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.
PTS: 1

REF: Page 1450 | Box 41-5

28. The most common clinical manifestation of portal hypertension is what type of bleeding?
a. Rectal
c. Esophageal
b. Duodenal
d. Intestinal
ANS: C

The vomiting of blood from bleeding esophageal varices is the most common clinical
manifestation of portal hypertension.
PTS: 1

REF: Page 1453

29. What is the most common manifestation of portal hypertensioninduced splenomegaly?

a. Leukopenia
c. Erythrocytopenia
b. Thrombocytopenia
d. Pancytopenia
ANS: B

Thrombocytopenia (decreased platelet count) is the most common manifestation of congestive

splenomegaly and can contribute to a tendency of increased bleeding.
PTS: 1

REF: Page 1452

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.

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.
PTS: 1

REF: Page 1453

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.
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.
PTS: 1

REF: Pages 1454-1455

32. Hepatic fat accumulation is observed in which form of cirrhosis?

a. Biliary
c. Postnecrotic
b. Metabolic
d. Alcoholic
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.
PTS: 1

REF: Pages 1460-1461

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.
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.
PTS: 1

REF: Pages 1460-1462

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.
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.
PTS: 1

REF: Page 1464

35. The mutation of which gene is an early event associated with the pathogenetic origin of

esophageal cancer?
a. K-ras mutation
b. TP53

c. myc
d. HER2

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.
PTS: 1

REF: Page 1466

36. Obesity is defined as a body mass index (BMI) greater than what measurement?
a. 22
c. 28
b. 25
d. 30
ANS: D

Obesity is an energy imbalance, with caloric intake exceeding energy expenditure, and is
defined as a BMI greater than 30.
PTS: 1

REF: Page 1446

MULTIPLE RESPONSE
37. Which statements are true regarding parietal pain? (Select all that apply.)
a. Parietal pain arises from the parietal peritoneum.
b. It is generally more localized than visceral pain.
c. Parietal pain is usually less intense than visceral pain.
d. Nerve fibers that travel to the spinal cord are involved in parietal pain.
e. Parietal pain corresponds to dermatomes T6 and L1.
ANS: A, B, D, E

Parietal pain arises from the parietal peritoneum and is more localized and intense than
visceral pain. Nerve fibers from the parietal peritoneum travel with peripheral nerves to the
spinal cord, and the sensation of pain corresponds to skin dermatomes T6 and L1.
PTS: 1

REF: Page 1426

38. Which statements are true regarding chronic gastritis? (Select all that apply.)
a. Chronic gastritis tends to occur in older adults.
b. It causes thinning and degeneration of the stomach wall.
c. Chronic gastritis results in chronic inflammation and mucosal atrophy.
d. Mucosal atrophy is a common outcome of chronic gastritis.
e. Epithelial metaplasia is often observed with chronic gastritis.
ANS: A, C, D, E

Chronic gastritis tends to occur in older adults and causes chronic inflammation, mucosal
atrophy, and epithelial metaplasia. Neither thinning nor degeneration of the stomach wall is
associated with chronic gastritis.
PTS: 1

REF: Page 1434

39. Which hormones are natural appetite suppressants? (Select all that apply.)
a. Insulin
b. Cortisol
c. Galanin
d. Calcitonin
e. Serotonin
ANS: A, D, E

Insulin, calcitonin, and serotonin are natural appetite suppressants, whereas cortisol and
galanin are natural appetite stimulants.
PTS: 1

REF: Page 1448 | Box 41-4

40. Which are the early (prodromal) clinical manifestations of hepatitis? (Select all that apply.)
a. Fatigue
b. Vomiting
c. Itching
d. Splenomegaly
e. Hyperalgia
ANS: A, B, E

The prodromal (preicteric) phase of hepatitis begins approximately 2 weeks after exposure
and ends with the appearance of jaundice. Fatigue, anorexia, malaise, nausea, vomiting,
headache, hyperalgia, cough, and low-grade fever are prodromal symptoms that precede the
onset of jaundice. Itching and splenomegaly are not associated with the prodromal phase of
hepatitis.
PTS: 1

REF: Page 1459

41. Which clinical manifestations are consistent with cancer of the cecum and ascending colon?

(Select all that apply.)

Mahogany-colored blood mixed with stool
Anemia
Pain
Constipation
Palpable mass in the lower right quadrant

a.
b.
c.
d.
e.

ANS: A, B, C, E

Clinical manifestations consistent with cancer of the cecum and ascending colon include pain,
a palpable mass in the lower right quadrant, anemia, and dark red or mahogany-colored blood
mixed with the stool. Constipation is not associated with this diagnosis.
PTS: 1

REF: Page 1471

MATCHING

Match the descriptions with the corresponding terms.

______ A. Ulcerative colitis
______ B. Crohn disease
42. Alterations in immunoglobulin G (IgA) production have been found in individuals with this

disorder.
43. Inflammation develops in crypts of Lieberkhn in the large intestine.
42. ANS: B
PTS: 1
REF: Page 1442
MSC: In Crohn disease, elevations in IgG are associated with the severity of the disease.
43. ANS: A
PTS: 1
REF: Page 1441
MSC: Inflammation begins at the base of the crypts of Lieberkhn in the large intestine, primarily the
left colon, with infiltration and release of inflammatory cytokines from neutrophils, lymphocytes,
plasma cells, macrophages, eosinophils, and mast cells.