ADVENTIST UNIVERSITY OF THE PHILIPPINES BLOCK

COLLEGE OF MEDICINE
Class of2020 222
CMED 222- QUIZ 1 RECALLS
Ref: GI Physiology: Secretion Lecture S# 29 (Dr. Berto)
TOPIC Week 1
LECTURER Dr. Delafuente, Dr. Felicen, Dr. 4. Which of the following is important in activating one or more
Berto proteolytic enzymes, converting them into an active form?
DATE February 21, 2018 Trypsin Enterokinase Pepsin
MASTER- Bollong, Cabral, Ramos, Vicente A. No No No
BATES B. No No Yes
C. No Yes No
1. Gastric acid...What factors have a direct action on the parietal D. Yes Yes Yes
cells to stimulate acid secretion?
Gastrin Somatostatin Acetylcholine Histamine Answer: D. Yes Yes Yes
When first synthesized in the pancreatic cells, the proteolytic digestive
A. No No Yes Yes
enzymes are in their enzymatically inactive forms trypsinogen,
B. Yes No No Yes chymotrypsinogen, and procarboxypolypeptidase. They become activated
C. Yes No Yes Yes only after they are secreted into the intestinal tract. Trypsinogen is
D. Yes Yes Yes Yes activated by an enzyme called enterokinase, which is secreted by the
E. Yes Yes No Yes intestinal when chime comes in contact with mucosa.
Ref: Guyton and Hall: Medical Physiology 13th ed. p781
Answer: C. Yes No Yes Yes
Three substances stimulate H+ secretion by gastric parietal cells: 5. Gastric Phase accounts for about 60% of acid response to meal.
histamine (a paracrine), ACh (a neurocrine), and gastrin (a hormone). Each Which substance can virtually eliminate the secretion of acid
substance binds to a different receptor on the parietal cell and has a during gastric phase?
different cellular mechanism of action. In addition, there are indirect A. Antacids
effects of ACh and gastrin via stimulation of histamine release. B. PPI
Ref: GI Physiology: Secretion Lecture S# 33 (Dr. Berto) C. Atropine
D. Histamine H2 Blockers
2. Cystic Fibrosis is a common cause of pancreatitis in children.
Which of the following explains this? Answer: B. PPI
A. Activation of enterokinase
B. Activation of trypsin inhibitor
C. Auto digestion of pancreas
D. Gallstone obstruction

Answer: C. Auto digestion of pancreas

Chronic pancreatitis in children is often caused by genetic mutations or by
congenital anomalies of the pancreatic or biliary ductal system. Mutations
in the PRSS1 gene (cationic trypsinogen) located on the long arm of
chromosome 7, in SPINK 1 gene (pancreatic trypsin inhibitor) located on
chromosome 5, in the cystic fibrosis gene (CFTR), and in the chymotrypsin
C gene (CTRC) may all lead to chronic pancreatitis. Cationic trypsinogen
has a trypsin-sensitive cleavage site. Loss of this cleavage site in the
abnormal protein permits uncontrolled activation of trypsinogen to
trypsin, which leads to auto digestion of the pancreas.
Ref: Nelson’s essential to pediatrics 20th ed. p.2777
Omeprazole is a proton pomp inhibitor.
3. Proenzyme pepsinogen is secreted by what cell? Ref: GI Physiology: Secretion Lecture S# 38 (Dr. Berto)
A. Chief cells
B. Ductal cells pf pancreas 6. 68 year old, Female, with hematemesis heartburn and stomach
C. Epithelial cells of duodenum pain. Endoscopy= + gastric inflammation including the body and
D. Acinar cells of pancreas antrum +small gastric ulcer + h pylori in biopsy. H pylori damages
the gastric mucosa by increasing the levels of:
Answer: A. Chief cells A. Ammonium
B. Bile salts
C. Gastrin
D. Pepsin

Answer: A. Ammonium
The bacterium is capable of penetrating the mucosal barrier by virtue of
its physical capability to burrow through the barrier and by releasing
ammonium that liquefies the barrier and stimulates the secretion of
hydrochloric acid. As a result, the strong acidic digestive juices of the
stomach secretions can then penetrate into the underlying epithelium and
literally digest the gastrointestinal wall, thus leading to peptic
Ulceration
Ref: Guyton and Hall: Medical Physiology 13th ed. p844

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7. Factors stengthen/weaken gastric mucosal barrier: bile salts Answer: A. Hypotonic relative to plasma
mucus NSAIDS gastrin ethanol (1) High volume (relative to the small size of the salivary glands)
Bile Salts Mucus NSAIDS Gastrin Ethanol (2) High K + and HCO3– concentrations
A. + + - + + (3) Low Na+ and Cl– concentrations
B. + + - - + (4) Hypotonicity
C. - + - + - (5) Presence of α-amylase, lingual lipase, and kallikrein
D. - + - + + Ref: Dr. Berto’s GI Physiology lecture

Answer: 13. Duodenal ulcer managed with cemetidine

*Lacking one option: Aspirin A. Muscarinic
B. H2
8. Which site of secretion does Intrinsic Factor came from? C. Increased CAMP
A. Gastric antrum
D. Blocks ATPase
B. Gastric body
C. Duodenum
D. Ileum Answer: B. H2
See number 5 picture.
Answer: B. Gastric body Ref: Dr. Berto’s GI Physiology lecture
Pls. Refer to the image in #3.
14. When parietals cell are stimulated, they secrete:
9. A 49y/o with severe crohn’s disease is not responsive to drug A. HCl and intrinsic factor
therapy and undergoes ileal resection. After surgery, he will have B. HCl and pepsin
steatorrhea because :
C. Gastrin and pepsin
A. The liver bile acid pool increases
D. Gastrin and trypsin
B. Chylomicrons does not form in the intestinal lumen
C. Micelles does not form in the intestinal lumen
D. Pancreas does not secrete lipase Answer: A. HCl and intrinsic factor
See number 3 rationale.
Answer: C. Micelles does not form in the intestinal lumen Ref: Dr. Berto’s GI Physiology lecture
Ref: Rationale (Dr. JFelicen)
15. A patient with Zollinger ellison syndrome would be
10. Inhibited by low ph: expected to have the ff changes
A. Secretin A. Decreased gastrin levels
B. Gastrin B. Increased insulin
C. CCK
C. PUD
D. VIP
D. Decreased parietal cell mass
Answer: B. Gastrin
With food in the stomach, as H+ is secreted, much of it is buffered; the Answer: C. PUD
gastric contents are acidified, but not as much as they would be if there Triad of ZES:
were no buffers. When the food moves to the small intestine, the 1. Hypergastrinemia
buffering capacity is reduced, and further H+ secretion reduces gastric pH 2. Gastrinoma
to even lower values. This lower pH then inhibits gastrin secretion, which 3. PUD
decreases H+ secretion.
Ref: Harrison’s Principles of Internal Medicine
Ref: GI Physiology: Secretion Lecture S# 38 (Dr. Berto)
16. Atresia of the esophagus is often associated with
11. Micelles are essential in the intestinal digestion of: A. Esophageal webs
A. Glycerol B. Trachel fistula
B. Galactose C. Pyloric stenosis
C. Vit B12 D.
D. Vit. D
Answer: B. Trachel fistula
Answer: D. Vit. D Atresia occurs most commonly at or near the tracheal bifurcation
Transport of lipids - Bile salts carry lipids (monoglycerides, fatty
and usually is associated with a fistula connecting the upper
acids, cholesterol, others) to intestinal wall in the form of micelles. or lower esophageal pouches to a bronchus or the trachea.
Vit D is the only fat soluble substance in the choices. Ref: Robbin’s Basic Pathology pp. 558
Ref: Dr. Berto’s GI Physiology lecture
17. The characteristic histologic feature of achalasia is which
12. Which of the following in characteristics of saliva? of the following?
A. Hypotonic relative to plasma A. Destruction of ganglion cells
B. Low HCO3 concentration than plasma B. Hypertrophy of muscular layer
C. Prescence of Proteases C. Hypertrophy of nerve bundles
D. Secretion rate increased by vagotomy D. Fibrosis of involve segment

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 D. Pepsin
Answer: A. Destruction of ganglion cells
Degenerative changes in neural innervation, either intrinsic to the Answer: B. HCL
esophagus or within the extraesophageal vagus nerve or the As rationalized by Doc ERF
dorsal motor nucleus of the vagus, also may occur. Ref: Dr, ERF’s statement in the ratio
Ref: Robbin’s Basic Pathology pp. 558
23. Initial response of esophageal epithelium to persistent
18. Physiologic Change in the Esophageal Sphincter in gastric content reflux
Achalasia A. Hyperplasia of squamous cell epithelium
A. Persistent Dilatation B. Columnar metaplasia
B. Loss of protective Mucosal Barrier C. Goblet cell metaplasia
C. Uncoordinated Peristalsis D. Ulceration
D. Failure to Relax
Answer: A. Hyperplasia of squamous cell epithelium
Answer: D. Failure to Relax As rationalized by Doc ERF
3.1.1. Achalasia – uncommon condition wherein the lower Ref: Dr, ERF’s statement in the ratio
esophagus loses its coordinated muscle contraction associated
with a sluggish or failure of the lower esophageal sphincter to
24. Incident of Barret’s Esophagus is higher in
relax (cardospasm)
Ref: Dr. ERF’s GIT syllabus pp3.
A. Smoking
B. Alcohol
19. The most prominent initial clinical manifestation of C. Hiatal Hernia
patients with Achalasia is: D. Pregnancy
A. Vomiting
B. Epigastric pain Answer: C. Hiatal Hernia
C. Bleeding As rationalized by Doc ERF
Ref: Dr, ERF’s statement in the ratio
D. Dysphagia

Answer: D. Dysphagia 25.In the Americans, it is essential in histopathologic

Mainly seen in middle ages; dysphagia is a prominent clinical diagnosis of Barret esophagus
symptom. A. Columnar cells
Ref: Dr. ERF’s GIT syllabus pp3 B. Intestinal metaplasia
C. Goblet cells
20. In obstruction of portal vein, esophageal varices can D. Basal cell metqplasia
develop because of this vascular channel
A. Right gastric vein Answer: C. Goblet cells
B. Esophageal plexus of veins As rationalized by Doc ERF
C. Left gastric vein Ref: Dr, ERF’s statement in the ratio
D. Splenic vein
26. How many percent of patients with barrett esophagus
Answer: C. Left gastric vein would develop adenocarcinoma?
Left gastric vein is the main branch of portal vein going to A. 0.5-1%
esophagus. B. 5%
Ref: Doc ERF’s statement C. 5-10%
D. >10%

21. Eosinophillic esophagitis is frequently associated with Answer: A. 0.5-1%

which of the following As rationalized by Doc ERF
A. Eczema Ref: Dr, ERF’s statement in the ratio
B. Asthma
C. Food allergies 27. Triggers the pathogenesis of adenocarconoma arising
D. All of the above from a background of Barrett's Esophagus.
a. Columnar cell metaplasia
Answer: D. All of the above b. Reflux esophagitis
As rationalized by Doc ERF c. Dysplasia
Ref: Dr, ERF’s statement in the ratio d. Hyperplasia of squamous epithelium

22. Essential for pathogenesis of reflux esophagitis Answer: C. Dysplasia

A. Destruction of the mucus protection of esophagus As rationalized by Doc ERF
B. HCL Ref: Dr, ERF’s statement in the ratio
C. Bile salts

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28. Adenocarcinoma of esophagus D. Antrum
A. Upper segment
B. Middle third Answer: C. Body
C. Lower third Ref: Dr. Erf Delafuente’s rationale
D. No site predilection
34. Anemia associated with autoimmune chronic gastritis?
Answer: C. Lower third
As rationalized by Doc ERF A. Fanconi’s anemia
Ref: Dr, ERF’s statement in the ratio B. Megaloblastic anemia
C. Iron deficiency anemia
29. Squamous Cell Carcinoma of the esophagus is more
D.
common in this segment
A. Gastroesophageal junction
B. Middle 3rd Answer: B. Megaloblastic anemia
C. Lower 3rd Ref: Dr. Erf Delafuente’s rationale
D. No site predilection
35. H. pylori gastritis is most often initiated in this part of the
Answer: B. Middle third stomach?
As rationalized by Doc ERF A. Gastroesophageal junction
Ref: Dr, ERF’s statement in the ratio
B. Cardia
30.Which of the following is essential in the maintenance of C. Body
the protective mucosal barrier? D. Anthrum
A. Integrity of tight junctions
B. Impermeability of the lyminal membrane Answer: D. Anthrum
C. Adequate mucosal blood supply Ref: Dr. Erf Delafuente’s rationale
D. Mucus secretion
36. The reason why H. pylori do not affect mucosal barrier?
Answer: C. Adequate mucosal blood flow
As rationalized by Doc ERF A. Less virulence factor of CagA
Ref: Dr, ERF’s statement in the ratio B. Bateria is killed by acid and pepsin
C. Insufficient adhesion
31. Acute bleeding in Chronic Gastritis is initiated by D. Lack of urease production
A. Chronic ulcer
B. Acute erosion Answer: A. Less virulence factor of CagA
Ref: Dr. Erf Delafuente’s rationale
C. Increase vascular permeability
D. M
37. Enables H.pylori to reach the surface of the epithelium of
the stomach
Answer: B. Acute erosion
Ref: Dr. Erf Delafuente’s rationale A. Organism is flagellated
B. Secretion of cytotoxines
32. Autoimmune chronic gastritis is associated with C. Ability to produce urease
antibodies against which of the ff? D. Diminished mucous secretion
A. Surface foveolar cells
B. Parietal cells Answer: C. Ability to produce urease
Ref: Dr. Erf Delafuente’s rationale
C. Gundic glands
D. Mucosal
38. WHO classified H. pylori as carcinogen because of this property:
A. Ability to integrate its genome into the epithelial cells
Answer: B. Parietal cells B. Presence of urease
Ref: Dr. Erf Delafuente’s rationale C. Presence of cag-a
D. Presence of adhesion molecules
33. Autoimmune chronic gastritis involves this portion of the
Answer: C. Presence of cag-a
stomach H. pylori organisms have adapted to the ecologic niche provided by gastric
A. GEJ mucus. Its virulence is linked to factors: Toxins, such as cytotoxin-
associated gene A (CagA), that may be involved in disease progression.
B. Cardia Ref: Robbins & Cotran Pathologic Basis of Disease.p.763
C. Body

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39. What advice would you asymptomatic benign esophageal sequence from chronic gastritis.
lesion? A. Atrophy > intestinal metaplasia > dysplasia
A. Observe; minimal risk to evolve to malignant anyway B. Intestinal metaplasia > atrophy > dysplasia
B. FNAB to ensure if it is benign C. Atrophy > intestinal metaplasia > dysplasia
C. Renucleation D. Atrophy > dysplasia > intestinal metaplasia
D. All of the above
Answer: A/C. Atrophy > intestinal metaplasia > dysplasia
Answer: A. Observe; minimal risk to evolve to malignant
anyway
Ref: Rationale from Dr. Felicen

40. Histology of peptic gastric ulcer that indicates that process is

chronic:
A. Mononuclear cell
B. Layers of necrotic debris
C. Granulation tissue
D. Fibrosis

Answer: D. Fibrosis
Ref: Pathology of GI: Stomach Lecture S#96 (Dr. Dela Fuente)

44. Most common site gastric adenocarcinoma:

A. Cardia
B. Body
C. Antrum
D. Pyloro-duodenal junction

Mechanisms of gastric injury and protection. This diagram illustrates the
progression from more mild forms of injury to ulceration that may occur
with acute or chronic gastritis. Ulcers include layers of necrosis (N),
inflammation (I), and granulation tissue (G), but a fibrotic scar (S), which
takes time to develop, is only present in chronic lesions.
Ref: Robbins & Cotran Pathologic Basis of Disease.p.761
41. The more common intestinal type of gastric adenocarcinoma is
associated with this gene mutation?
A. E cadherin
B. Her2/Neu
C. P53
D. Kras
Answer: B. Her2/Neu
Answer: C. Antrum
Most gastric adenocarcinomas involve the gastric antrum; the lesser
curvature is involved more often than the greater curvature.
Ref: Robbins & Cotran Pathologic Basis of Disease.p.772
45. Most common type of symptom arising on a background of H.
pylori gastric lymphoma
A. Hodgkin
B. T-cell
C. B-cell
D. NK type
Answer: C. B-cell
Nearly 5% of all gastric malignancies are primary lymphomas, the most
common of which are indolent extranodal marginal zone B-cell
lymphomas. In the gut these tumors are often referred to as lymphomas
of mucosa-associated lymphoid tissue (MALT), or MALTomas.
Ref: Robbins & Cotran Pathologic Basis of Disease.p.773

46. The most common type of intestinal lymphoma arising on the

background of celiac disease:
A. Hodgkin
B. T cell
C. B cell
D. NK type

Ref: Pathology of GI: Stomach Lecture S#98 (Dr. Dela Fuente) Answer: B. T cell

42. The above gene causes which of the following pathogenesis of

gastric adenocarcinoma?
A. Disrupt the normal adhesion between epithelial cells
B. Prevents repair of gene mutation
C. Overexpression of EGF receptor
D. Disrupts the normal signaling pathway

Answer: C. Overexpression of EGF receptor

Ref: Rationale from Dr. Dela Fuente

43. Gastric adenocarcinoma initiated by H. pylori goes thru this

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 The left panel illustrates the morphologic alterations that may be present
celiac disease. The right panel depicts a model for the pathogenesis of
51. Which statement best describes the narrowest
celiac disease. Note that both innate (CD8+ intraepithelial T cells,
activated by IL 15) and adaptive (CD4+ T cells, and B cells sensitization to esophageal constriction:
gliadin) immunemechanisms are involved in the tissue responses to A. Uppermost constriction brought about by the
gliadin. gastroesophageal mechanism
Ref: Robbins & Cotran Pathologic Basis of Disease.p.773
B. Middle constriction due to crossing of left mainstem
47. Absent in hirshsprung's disease brochus and arch of aorta
A. Nerve bundles
C. Variable diameter caused by the cricopharyngeal
B. Muscular layer
C. Hypoplastic ganglion cells muscle
D. Auerbach ganglion cells D. Has a luminal diameter of 1.5 cm

Answer: D. Auerbach ganglion cells Answer: D. Has a luminal diameter of 1.5 cm

Hirschsprung disease, also known as congenital aganglionic megacolon, UPPERMOST:
results when the normal migration of neural crest cells from cecum to -Cricopharyngeal muscle
rectum is arrested prematurely or when the ganglion cells undergo -1.5cm diameter
premature death. This produces a distal intestinal segment that lacks both
-*narrowest
the Meissner submucosal and the Auerbach myenteric plexus
Ref: Dr. Felicen’s Esophagus lecture
(“aganglionosis”). Coordinated peristaltic contractions are absent and
functional obstruction occurs, resulting in dilation proximal to the affected
segment. 52. Blood supply of upper esophagus
Ref: Robbins & Cotran Pathologic Basis of Disease.p.772 A. inferior thyroid artery
B. –
48. The initial response for typhoid is: C.—
A. Apthous ulcers in intestine D. –
B. Ulceration in ileum
C. Erosion of surface epithelium Answer: A. inferior thyroid artery
D. Hyperplasia of Peyer patches

Answer: D. Hyperplasia of Peyer patches

Typhoid fever
Pathology: enlarged Peyer patches leading to necrosis and
ulceration; oval ulcers parallel to long axis of ileum
Ref: GIT syllabus pp. 20

49. The initial flask shaped ulcers of amoebic colitis are due to
the organism ‘s:
A. Inability to penetrate the muscularis propia
B. Capability to cause mucosal ischemia
C. Attachment in epithelial cells
D. AOTA

Answer: A. Inability to penetrate the muscularis propia Ref: Dr. Felicen’s Esophagus lecture
 Trophozoites secrete cytolytic enzymes enabling the them to
pass through the lining epithelium of the crypts and into the 53. In portal venous obstruction , what serves as a collateral
lamina propria causing necrosis; mostly liquefactive necrosis pathway for portal blood to enter the SVC through azygous
 Necrosis does not progress beyond the muscularis mucosae; veins
it then extends out laterally creating a small flask-shaped A. Esophageal plexus of veins
ulcer B. Cappilaries of the esophagus
Ref: GIT syllabus pp 22
C. Submucosal venous plexus
D. Paraesophageal venous plexus
50. Initiating cause of appendicitis
A. Ulceration Answer: C. Submucosal venous plexus
B. Ischemia The submucosal venous networks of the esophagus and stomach
C. Luminal obstruction are in continuity with each other, and, in patients with portal
D. Bacterial overgrowth venous obstruction, this communication functions as a collateral
pathway for portal blood to enter the superior vena cava via the
Answer: C. Luminal obstruction azygos vein.
Acute appendicitis is most common in children and adolescents. It Ref: Dr. Felicen’s Esophageal diseases of adulthood lecture
is thought to be initiated by increased intraluminal pressure
consequent to obstruction of the appendiceal lumen, which 54. At rest, the esophagus is in relaxed state except for the
compromises venous outflow. esophageal sphicter, which resting pressures are
Ref: Robbins Basic pathology pp 601 approximately:

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 A. 0-15 mmHg Answer: D. A and C
B. 10-20 mmH2O Collis Gastroplasty + Fundoplication are used in esophageal
C. 15-30 mmHg shortening from chronic severe GERD
Ref:Dr.JFelicenEsophagealDisorders...ppt.,slide28
D. 15-30 mmH2O

Answer: C. 15-30 mmHg 60. Distant organs commonly involved in esophageal CA

Resting pressures of the UES & LES: 15-30mmhg A. Liver and bone
Ref: Dr. Felicen’s Esophageal diseases of adulthood lecture B. Brain and bone
C. Liver and lung
55. Difficulty swallowing D. Brain and lung
A. Dysphagia
B. Achalasia Answer: C. Liver and Lung
C. Odynophagia Distant organs most commonly involved in esophageal CA are
D. Globus hystericus liver and lungs
Ref:Dr.JFelicenEsophagealDisorders...ppt.,slide32
Answer: A. Dysphagia
Dysphagia 61. Tumor location is used only for staging of which tissue
type esophageal CA
solids) from mouth to stomach A. Squamous CA
Ref: Dr. Felicen’s Esophageal diseases of adulthood lecture B. Adenocarcinoma
C. Both
56. Late complications of GERD, EXCEPT: D. Neither
A. Pyrosis
B. Schatki's ring Answer: A. Squamous CA
C. Barett's esophagus Tumor location used only for the staging of SCCa
D. NOTA Ref: Ref:Dr.JFelicenEsophagealDisorders...ppt.,slide35 NOTES

Answer: A. Pyrosis
Complications of gastroesophageal reflux such as 62. Esophageal CA, T3N0M0
esophagitis, stricture, and Barrett’s metaplasia A. Stage IIA
Ref: Dr. Felicen’s Esophageal diseases of adulthood lecture B. Stage IIB
C. Stage IIIA
57. The following are included in the medical management of D. Stage IIIB
GERD except:
A. Weight reduction and modification of eating habits Answer: B. Stage IIB
B. Assumption of proper body posture In case of adenocarcinoma, T3N0M0 is under stage IIB but in
C. Avoidance of caffeinated and alcoholic drinks case of squamous cell Ca, T3N0M0 can be under stage IIA or
D. Anticholinergic, beta-blockers, xanthine stage IIB
Ref: Ref:Dr.JFelicenEsophagealDisorders...ppt.,slide36-37
Answer: D. Anticholinergic, beta-blockers, xanthine
Ref: Dr. Felicen’s statement 63. Over-all survival rate of patients with esophageal CA.
A. 20%
58. Which of the following is/are a good predictor of B. 40%
successful response to surgery? C. 60%
A. Positive pH test D. 80%
B. Reflux symptoms
C. Symptomatic relief with PPIs Answer: A. 20%
D. All of the above Overall 5 year survival rate for surgical treatment of esophageal
CA is 20%
Ref:Dr. JFelicen Esophageal Disorders...ppt.,slide39
Answer: D. All of the above
All are predictors of successful response to surgery
Ref:Dr.JFelicenEsophagealDisorders...ppt.,slide25 64. Most frequently used conduit as esophageal substitute:
A. colon
59. Patient with shortened esophagus due to severe chronic B. ileum
GERD. What surgical intervention? C. jejunum
A. Collitis gastroplasty D. stomach
B. Nissen
C. Fundoplication Answer: D. stomach
D. A and C Stomach is the most frequently used conduit for esophageal
resection
Ref:Dr.JFelicen’s Esophageal Disorders...ppt.,slide40

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 Type 1 Sliding hiatal hernia – frequently associated
65. Neoadjuvant therapy with GERD
A. to downstage tumor GEJ slides in and out of the chest through
B. To improve cancer survival after resection esophageal hiatus
C. To prevent metastases to distant organs Type II Paraesophageal hernia – isolated stomach
prolapse thru a weak phrenoesophageal
D. A and B
ligament, GEJ preserved in the abdomen
Type III Sliding + Paraesophageal hernia
Answer: D. A and B
Type IV Herniation of other organs (eg. Colon, spleen)
A and B are the only reasons of doing neoadjuvant therapy
Ref: Dr. CFelicen’s Disease & Disorders of Esophagus slide 53
Ref:Dr.JFelicenEsophagealDisorders...ppt.,slide45

66. When is surgery recommended after a patient is done 70. Management for symptomatic type II hernia
with neoadjuvant therapy? A. Reduction of hernia
A. 4 weeks after treatment B. Diaphragnatic defect reconstruction
B. 6-7 weeks after treatment C. Fundoplication and gastropexy
C. 3-6 weeks after treatment
D. All of the above
D. Immediately after completion of treatment

Answer: A. 4 weeks after treatment Answer: D. All of the above

Surgery is indicated 4 weeks after completion of Surgery repair is indicated for symptomatic type II Hernia and is
neoadjuvant treatment done by the ff:
Ref:Dr.JFelicenEsophagealDisorders...ppt.,slide45 - Reduction of Hernia
- Reconstruction of diaphragmatic defect
- Fundoplication
67. In advanced esophageal adenocarcinoma, complications - Anchoring of the stomach with
due to the use of stent as palliative management includes Gastrostomy tube/ Gastropexy
all of the following EXCEPT Ref: Dr. CFelicen’s Disease & Disorders of Esophagus slide 57
A. Perforation
B. Migration of stent
71. Diagnostic finding of Achalasia except:
C. Reflux
D. All of the above A. Hyperplasia of the distal esophagus on video
fluoroscopy
Answer: D. All of the above B. Bird’s beak on barium swallow
In palliative care, complications in the use of C. Esophageal pressure of <26 mmHg
stent include perforation, migration of stent,
reflux, and impaction of food
Ref: Dr. JFelicen Esophageal Disorders...ppt., slide 48 Answer: A. Hyperplasia of the distal esophagus on video
fluoroscopy
Ref: Dr. JFelicen’s rationale
68. Palliative care is giving a _________ quality of life in the
_________ time available for the patient. 72. Disorder of Esophageal movement characterized by
A. Limited, Aggressive contractions in the smooth muscle of the esophagus in a
B. Aggressive, Limited normal sequence but at an excessive amplitude or
C. Comfortable, Limited duration:
D. Limit, Comfortable A. Achalasia
B. Diffuse esophageal spasm
Answer: C. Comfortable, Limited C. Nutcracker esophagus
Ref: Dr. CFelicen’s Disease & Disorders of Esophagus slide 51 D. Hypertensive LES

69. GEJ slides in and out of chest thru esophageal hiatus: Answer: C. Nutcracker esophagus
A. Type I Nutcracker esophagus, also known as Hypertensive peristalsis,
B. Type II is a disorder of esophageal movement characterized by
C. Type III contractions in the smooth muscle of the esophagus in a
D. Type IV normal sequence but at an excessive amplitude or duration.
Symptoms include difficulty swallowing, or dysphagia, to both
solid and liquid foods.
Answer: Type I
Ref: Dr. CFelicen’s Disease & Disorders of Esophagus slide 57
HH Type Description

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73. True of Zenker's diveticulum, except:
A. Esophageal motility disorder
B. Traction diverticulum
C. Pulsion diverticulum
D. Affect the cervical esophagus
Answer: B. Traction diverticulum
Zenker’s diverticulum is a pulsion type diverticula that occurs in
the cervical esophagus causing cricopharyngeal muscle
dysfunction, this eventually leads to failure to relax on
swallowing causing proximal obstruction. It occurs posteriorly
(transition area of weakness) between hypopharynx and
esophagus, above cricopharyngeus muscles.
Ref: Dr. CFelicen’s Disease & Disorders of Esophagus slide 69
74. Associated with inflammatory paratracheal lymph node
disease associated with TB and or histoplasmosis
A. Traction diverticula
B. Epiphrenic diverticulum
C. Zenker’s diverticulum
D. All of the above
Answer: A. Traction diverticulum
Traction diverticulum is commonly associated with inflammatory
paratracheal LN disease associated with TB or Histoplasmosis. It
is usually asymptomatic and left alone. However, complication
such as fistula formation to trachea/ adjacent blood vessels can
happen leading to respiratory and bleeding problems.
Surgical Mngt: Excision of diverticula, Repair of adjacent
structure
To prevent recurrence/ promote healing: Interposition flap of
tissue is used
Ref: Dr. CFelicen’s Disease & Disorders of Esophagus slide 72
75. Most common benign esophageal neoplasms
A. Leiomyoma
B. Esophageal cysts
C. Granular cell tumor
D. Fibrovascupar polyp
Answer: A. Leiomyoma
Benign tumors of the esophagus are generally mesenchymal, and arise
within the esophageal wall, with leiomyomas being most common.
Fibromas,clipomas, hemangiomas, neurofibromas, and lymphangiomas
also occur.
Ref: Robbins & Cotran Pathologic Basis of Disease.p.758
76. Initiating cause for development of peptic ulcer of stomach
A. Increased acid production by hyperplastic parietal cells
B. Decreased mucus production by antral mucus glands
C. Persistent injury and necrosis of surface epithelial cells by acid
D. Decreased blood flow due to decreased prostaglandin
production
Answer: D. Decreased blood flow due to decreased
prostaglandin production
PUD has been associated with cigarette use and cardiovascular disease,
likely due to reduced mucosal blood flow, oxygenation, and healing.
Ref: Robbins & Cotran Pathologic Basis of Disease.p.767
COM 2020“Class with the perfect Vision” I can do all things through Christ who strengthens me Ph. 4:13
77. Immediate concern of esophageal injury:
A. Bleeding
B. Sepsis
C. Pneumothorax
D. Pain
Answer: B. Sepsis
Infection from cervical esophageal injury can rapidly extend to the
posterior mediastinum.
Ref. Esophageal Diseases and Disorders in adults Lecture (Dr. Felicen)
78. This causes perforation to the esophagus leading to
mediastinitis?
A. External trauma/Surgery
B. Foreign body
C. Instrumentation
D. Any of the above
Answer: D. Any of the above
Perforation of the esophagus constitutes a true emergency. It most
commonly occurs following diagnostic or therapeutic procedures.
Spontaneous perforation, referred to as Boerhaave’s syndrome, accounts
for only 15% of cases of esophageal perforation, foreign bodies for 14%,
and trauma for 10%. Pain is a striking and consistent symptom and
strongly suggests that an esophageal rupture has occurred, particularly if
located in the cervical area following instrumentation of the esophagus, or
substernally in a patient with a history of resisting vomiting.
Ref: Schwartz’s pricinple of Surgery 10th ed. p.1018
79. True of caustic ingestion, except:
A. Alkali dissolves tissue
B. Acids cause coagulative necrosis therefore penetrate more
C. Alkali are more frequently swallowed because strong acids can
cause immediate burning pain
D. Acids can be neutralized by milk, egg white and I forgot
Answer: B. Acids cause coagulative necrosis therefore penetrate
more
Alkalis are more frequently swallowed accidentally than acids, because
strong acids cause an immediate burning pain in the mouth. Alkalis
dissolve tissue, and therefore penetrate more deeply, while acids cause a
coagulative necrosis that limits their penetration. Lye or other alkali can
be neutralized with half-strength vinegar, lemon juice, or orange juice.
Acid can be neutralized with milk, egg white, or antacids.
Ref: Schwartz’s pricinple of Surgery 10th ed. p.1021
80. Most common site of dislodgment of foreign bodies:
A. Upper Esophagus
B. Mid Esophagus
C. Lower Esophagus
D A, B & C
Answer: A. Upper Esophagus
Upper most esophagus has the narrowest constriction diameter (1.5cm).
Ref. Esophageal Diseases and Disorders in adults Lecture (Dr. Felicen)
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