Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Internal Medicine > Part 14 - GIT > Flashcards

Part 14 - GIT Flashcards

1
Q

Disruption of the mucosal integrity of the stomach leading to a local defect or excavation due to active inflammation

A

Ulcer

p. 1911

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pyloric glands are found where?

A

Antrum

p. 1911

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The parietal cell is also known as?

A

oxyntic cell

p. 1911

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The parietal cell is usually found where?

A

Neck / isthmus / oxyntic gland

p. 1911

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The gastric epithelial lining consists of rugae that contain what?

A

Gastric pits

p. 1911

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where specifically does acid secretion occur?

A

Apical canalicular surface

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

First line of defense in the mucosal defense system?

A

Mucus-bicarbonate-phospholipid layer

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mucus is composed of what?

A

Water (95%) and mixture of phospholipids and glycoproteins (mucin)
(p. 1912)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Function of mucus

A

Impedes diffusion of ions and molecules (e.g. Pepsin)

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Forms a pH gradient ranging from 1 to 2 at the gastric luminal surface and reaching 6 to 7 along the epithelial cell surface

A

Bicarbonate

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the functions of the surface epithelial cells in the mucosal defense system?

A

1) Generate heat shock proteins that prevent protein denaturation
2) Generate trefoil factor family peptides and cathelicidins
3) Restitution
(p. 1912)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is restitution?

A

When gastric epithelial cells bordering a site of injury can migrate to restore a damaged region
(p. 1912)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which growth factors modulate the process of restitution?

A

Epidermal growth factor (EGF)
Transforming growth factor a (TGF-a)
Fibroblast growth factor (FGF)
(p. 1912)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which growth factors are important in regulating angiogenesis in the mucosal defense system?

A

Fibroblast Growth factor (FGF)
Vascular endothelial growth factor (VEGF)
(p. 1912)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is/are the function/s of prostaglandins in the mucosal defense system?

A

1) Regulate the release of mucosal bicarbonate and mucus
2) Inhibit parietal cell secretion
3) Maintain mucosal blood flow and epithelial cell restitution
(p. 1912)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

COX-1 is expressed what tissues?

A

Stomach, platelets, kidneys, endothelial cells

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

COX-2 is expressed in what cells?

A

Macrophages, leukocytes, fibroblasts, synovial cells

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Selective COX-2 inhibitors with adverse effect of myocardial infarction, therefore was removed from the market?

A

Valdecoxib and Rofecoxib

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the two principal gastric secretory products capable of inducing mucosal injury?

A

Hydrochloric acid and pepsinogen

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

HCl and pepsinogen play a role in the absorption of what nutrients/vitamins?

A

Iron, calcium, magnesium, vitamin B12

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Basal acid production occurs in a circadian pattern with the highest levels occurring during the _____.

A

Night

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the principal contributors to basal acid secretion?

A 
Cholinergic input (via vagus nerve)
Histaminergic input (from local gastric sources)
(p. 1912)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Stimulated gastric secretion occurs primarily in three phases, namely:

A

Cephalic
Gastric
Intestinal
(p. 1912)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

The GI hormone somatostatin is release from what cells?

A

Endocrine cells found in the gastric mucosa (D cells)

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Somatostatin is released in response to?

A

HCl

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How can somatostatin inhibit acid production directly and indirectly?

A

Directly via the parietal cell
Indirectly by decreased histamine release from ECL cells and gastrin release from G cells
(p. 1912)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hormone that may increase gastric acid secretion through stimulation of histamine release from ECL cells

A

Ghrelin

Pp. 1912-1913

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Ghrelin is expressed in what cell?

A

Gr cells in the stomach

p. 1912

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which cell secretes intrinsic factor (IF) and IL-11?

A

Parietal cell

p. 1913

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

The parietal cell expresses receptors for several stimulants of acid secretion, which includes:

A

Histamine (H2)
Gastrin (cholecystokinin B / gastrin receptor)
Acetylcholine (muscarinic, M3)
(p. 1913)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Histamine stimulates gastric acid secretion indirectly by?

A

Activating the histamine H3 receptor on D cells –> inhibits somatostatin release
(p. 1913)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Active catalytic site of the enzyme H+K+-ATPase is found within the ___ subunit

A

Alpha

p. 1913

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where are chief cells located?

A

Primarily in the gastric fundus

p. 1914

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What cell synthesizes and secretes pepsinogen and where is it found?

A

Chief cell - gastric fundus

p. 1914

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Pepsin activity is significantly diminished at a pH of?

A

4

p. 1914

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Pepsin activity is irreversibly inactivated and denatured at a pH of?

A

Greater than or equal to 7

p. 1914

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Ulcers are defined as?

A

Breaks in the mucosal surface >5 mm in size, with depth to the submucosa
(p. 1914)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the two most common risk factors for PUD?

A

Helicobacter pylori
NSAIDs
(p. 1914)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

___ ulcers tend to occur later in life with a peak incidence in the sixth decade of life.

A

Gastric

p. 1914

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Duodenal ulcers occur most often in which part of the duodenum?

A 
First part (>95%)
(p. 1914)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which type of ulcer should be biopsies upon discovery?

A

Gastric ulcers

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Where are benign gastric ulcers most often found?

A

Distal to the junction between the antrum and the acid secretory mucosa
(p. 1915)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How many types of gastric ulcer are there?

A

4

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Which type of gastric ulcer occur in the gastric body and tend to be associated with low gastric acid production?

A

Type I

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Which type of gastric ulcer occur in the antrum and gastric acid can vary from low to normal?

A

Type II

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Which type of gastric ulcer occur within 3 cm of the pyloric and are commonly accompanied by DUs and normal or high gastric acid production?

A

Type III

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Which gastric ulcer is found in the cardio and is associated with low gastric acid production?

A

Type IV

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Where is a Type I gastric ulcer located?

A

Gastric body

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Where is a Type II gastric ulcer located?

A

Antrum

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Where is a Type III gastric ulcer located?

A

Within 3 cm of the pylorus

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Where is a Type IV gastric ulcer located?

A

Cardia

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which type of gastric ulcer is the only one associated with high gastric acid secretion?

A

Type III

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

H. Pylori plays a role in the development of which conditions?

A

Peptic Ulcer Disease (PUD)
Gastric mucosa-associated lymphoid tissue (MALT) lymphoma
Gastric adenocarcinoma
(p. 1915)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

H. Pylori was initially called?

A

Campylobacter pyloridis

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Two factors that predispose to higher colonization rates of H. Pylori

A

Poor socioeconomic status
Less education
(p. 1915)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Risk factors for H. Pylori infection

A

Birth or residence in a developing country
Domestic crowding
Unsanitary living conditions
Unclean food or water
Exposure to gastric contents of an infected individual
(p. 1915)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Transmission of H. Pylori

A

Oral-oral
Fecal-oral
(p. 1915)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

H. Pylori is present in how many % of individuals with gastric ulcers?

A

30-60%

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

H. Pylori is present in how many % of individuals with duodenal ulcers?

A

50-70%

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Which specific region of the bacterial genome encodes the virulence factors Cag A and pic B?

A

cag-PAI

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Which virulence factor targets human CD4 T cells, inhibits their proliferation and disrupts normal function of B cells, CD8 T cells, macrophages, and mast cells?

A

Vac A

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

H. Pylori strains that are ____ positive are associated with higher risk of PUD, premalignant gastric lesions, and gastric cancer

A

Cag-PAI

p. 1915

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Which enzyme allows the H. Pylori bacteria to reside in the acidic stomach?

A

Urease

p. 1916

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How does urease allow the H. Pylori bacteria to reside in the stomach?

A

It generates NH3, which can damage epithelial cells

p. 1916

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Elevated concentrations of multiple cytokines are found in the gastric epithelium of H. Pylori-infected individuals, namely:

A 
IL-1a/B
IL-2
IL-6
IL-8
TNF-a
IFN-Y
(p. 1916)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

The presence of antral-predominant gastritis is associated with ___ ulcer.

A

Duodenal

p. 1916

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Gastritis involving the corpus predisposes to development of ___ ulcer.

A

Gastric

p. 1916

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Risk factors for NSAID-induced ulcer

A 
Advanced age
History of ulcer
Use of glucocorticoids, high-dose NSAIDs, multiple NSAIDs
Use of anticoagulants/clopidogrel
Serious multi system disease
(p. 1917)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Chronic disorders shown to have a STRONG association with PUD

A 
Advanced age
Chronic pulmonary disease
Chronic renal failure
Cirrhosis
Nephrolithiasis
A1-antitrypsin deficiency
Systemic mastectomies
(p. 1917)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Disorders with a POSSIBLE association with PUD

A 
Hyperparathyroidism
Coronary artery disease
Polycythemia vera
Chronic pancreatitis
Former alcohol use
Obesity
African-American race
3 or more doctor visits in a year
(p. 1917)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Typical abdominal pain pattern of duodenal ulcer

A

Occurs 90 minutes to 3 hours after a meal
Frequently relieved by antacids or food
Pain that awakens the patient from sleep (between 12 mn-3am)
(p. 1918)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Most discriminating symptom of duodenal ulcer

A

Pain that awakens the patient from sleep (between 12mn-3am)

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

In PUD, elderly patients are less likely to have abdominal pain and may instead present as?

A

Bleeding or perforation

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the most frequent PE finding in patients with gastric/duodenal ulcers?

A

Epigastric tenderness

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

PE of patient with gastric/duodenal ulcer: A severely tender, board-like abdomen suggests?

A

Perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Presence of succussion splash suggests?

A

Gastric outlet obstruction

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the most common complication observed in PUD?

A

GI Bleeding

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

GI bleeding as a complication of PUD occurs in how many percent of individuals?

A

15%

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the second most common complication of PUD?

A

Perforation

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Perforation as a complication of PUD occurs in how many percent of individuals?

A

6-7%

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

___ is a form of perforation in which the ulcer bed tunnels into an adjacent organ.

A

Penetration

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Duodenal ulcers tend to penetrate where?

A

Posteriorly into the pancreas

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Gastric ulcers tend to penetrate where?

A

Left hepatic lobe

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the least common PUD-related complication?

A

Gastric outlet obstruction

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Gastric outlet obstruction as a complication of PUD occur in how many percent of individuals?

A

1-2%

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

This refers to a group of heterogenous disorders typified by upper abdominal pain without the presence of an ulcer

A

NUD / functional dyspepsia / essential dyspepsia

p. 1918

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Appearance of a duodenal ulcer

A

Well-demarcated crater, most often seen in the bulb

p. 1919

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Appearance of a benign gastric ulcer

A

Discrete crater with radiating mucosal folds originating from the ulcer margin
(p. 1919)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Ulcers ___ in size or associated with a mass are more often malignant.

A

> 3 cm

p. 1919

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the most sensitive and specific approach for examining the upper GI tract (for PUD)

A

Endoscopy

p. 1919

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Specialized testing may be needed to be done in individuals with complicated or refractory PUD. Examples of which are:

A

Serum gastrin
Gastric acid analysis
Sham feeding
(p. 1919)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Infectious causes of ulcers not caused by H.pylori or NSAIDs

A

Cytomegalovirus
Herpes simplex virus
Helicobacter heilmannii
(p. 1918, Table 348-1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Drug/toxic causes of ulcers not caused by H.pylori and NSAIDs

A 
Bisphosphonates
Chemotherapy
Clopidogrel
Crack cocaine
Glucocorticoids (when combined with NSAIDs)
Mycophenolate mofetil
Potassium chloride
(p. 1918, Table 348-1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Invasive tests for detection of H.pylori

A

Rapid urease
Histology
Culture
(p. 1920)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Non-invasive tests for detection of H.pylori

A

Serology
Urea breath test
Stool antigen
(p. 1920, Table 348-2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Mainstay of treatment of PUD (non-pharmacological)

A

Eradication of H.pylori
Prevention of NSIAID-induced disease
(p. 1919)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Side effect of aluminum hydroxide

A

Constipation
Phosphate depletion
(p. 1920)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Side effect of magnesium hydroxide

A

Loose stools

p. 1920

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Magnesium-containing preparation (antacid) should not be used in chronic renal failure patients because?

A

Possible hypermagnesemia
Chronic neurotoxicity (due to aluminum)
(p. 1920)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Milk-alkali syndrome is caused by?

A

Long term use of calcium carbonate

p. 1920

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is milk-alkali syndrome?

A 
Hypercalcemia
Hyperphosphatemia
Possible renal calcinosis
Progression to renal insufficiency
(p. 1920)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

First H2 receptor antagonist used for treatment of acid peptic disorders

A

Cimetidine

p. 1920

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Which H2 receptor antagonist has a weak antiandrogenic effect resulting in reversible gynecomastia and impotence?

A

Cimetidine

p. 1920

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Which H2 receptor antagonists can bind to hepatic cytochrome P450?

A

Cimetidine
Ranitidine
(p. 1920)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Substituted benzimidazole derivatives that covalently bind and irreversibly inhibit H+,K+-ATPase

A

Proton pump inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Purposes of sodium bicarbonate in combination with PPIs:

A

1) Protect the Omeprazole from acid degradation
2) Promote rapid gastric alkalinization and subsequent proton pump activation
(p. 1920)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Half-life of PPIs

A

~18 hours

p. 1921

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Mechanism for rebound gastric hypersecretion after discontinuation of PPIs

A

Gastrin-induced hyperplasia and hyper trophy of histamine-secreting ECL cells
(p. 1921)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Long term acid suppression (esp. with PPIs) has been associated with a higher incidence of what conditions?

A

Community-acquired pneumonia
Community and hospital acquired Clostridium difficile-associated disease
(p. 1921)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

PPI containing an imidazopyridine ring instead of a benzimidazole ring, which promotes irreversible proton pump inhibition

A

Tenatoprazole

p. 1921

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

PPI that has a longer half-life and may be beneficial for inhibiting nocturnal acid secretion

A

Tenatoprazole

p. 1921

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Pharmacologic: complex sucrose salt in which the hydroxyl groups have been substituted by aluminum hydroxide and sulfate

A

Sucralfate

p. 1921

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Adverse effects of short term use of bismuth-containing compounds

A

Black stools
Constipation
Darkening of the tongue
(p. 1921)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Adverse effect of long term use of bismuth-containing compounds

A

Neurotoxicity

p. 1921

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

The Maastricht IV/Florence Concensus Report recommends that eradication of H.pylori should be considered in the ff:

A

1) First degree relatives of family members with gastric cancer
2) Patients with previous gastric neoplasm treated by endoscopic or subtotal resection
3) Patients with risk of gastritis or severe atrophy
4) On gastric acid inhibition for more than a year
5) Strong environmental risk factors for gastric cancer
6) H. Pylori positive with fear of gastric cancer
(p. 1922)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Risk factors for gastric cancer

A

Heavy smoking
High exposure to dust, coal, quartz, cement
Work in the quarries
(p. 1922)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

First triple regimen found effective against H.pylori

A

Bismuth, metronidazole, and tetracycline

p. 1922

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Failure of H.pylori eradication with triple therapy in a compliant patient is usually due to what?

A

Infection with a resistant organism

p. 1923

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What pharmacologic agent can heal gastric/duodenal ulcers independent of whether NSAIDs are discontinued?

A

PPIs

p. 1923

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

This study demonstrated that the advantage of Celecoxib in preventing GI complications was offset when low-dose aspirin was used simultaneously

A

CLASS study

p. 1923

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Treatment for gastric/duodenal ulcer caused by H.pylori?

A

Triple therapy for 14 days followed by continued acid-suppressing drugs (H2 blocker or PPI) for a total of 4-6 weeks
(p. 1924)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Test of choice for documenting eradication of H.pylori

A

Stool antigen test OR urea breath test

p. 1924

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

For gastric ulcer negative for neoplasm on initial endoscopy/biopsy, when should repeat endoscopy be done?

A

8-12 weeks

p. 1924

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

When is a gastric ulcer considered to be refractory to therapy?

A

If it fails to heal after 12 weeks of therapy

p. 1924

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

When is a duodenal ulcer considered to be refractory to therapy?

A

If it fails to heal after 8 weeks of therapy

p. 1924

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Signs and symptoms of EARLY dumping syndrome is due to what?

A

Rapid emptying of hyperosmolar gastric contents into the small intestine –> Fluid shift into the gut lumen –> plasma volume contraction and acute intestinal distention
(p. 1924)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

LATE phase of dumping syndrome is due to what?

A

Hypoglycemia from excessive insulin release

p. 1926

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Dumping syndrome is most noticeable after meals rich in ___.

A 
Simple carbohydrates (especially sucrose) and high osmolarity
(p. 1926)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Cornerstone of therapy for patients with dumping syndrome

A

Dietary modification

p. 1926

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Pathophysiology: Hypergastrinemia originating from an autonomous neoplasm

A

Zollinger-Ellison Syndrome

p. 1927

131
Q

Borders of the gastrinoma triangle

A

Superiorly - Confluence of the cystic and common bile ducts
Inferiorly - Junction of the second and third portions of the duodenum
Medically - Junction of the neck and body of the pancreas
(p. 1927)

132
Q

Most common clinical manifestation of ZES

A

Peptic ulcer

p. 1927

133
Q

Clinical situations that should create suspicion of gastrinoma

A

Ulcers in unusual locations (2nd part of duodenum and beyond)
Ulcers refractory to standard medical therapy
Ulcer recurrence after acid-reducing surgery
Ulcer presenting with frank complications
Ulcers in the absence of H.pylori or NSAID ingestion
(p. 1927)

134
Q

Second most common clinical manifestation of ZES

A

Diarrhea

p. 1927

135
Q

Gastrinomas can develop in the presence of what autosomal dominant disorder?

A

MEN 1 syndrome

p. 1927

136
Q

MEN 1 syndrome involves primarily what organ sites?

A

Parathyroid glands
Pancreas
Pituitary gland
(p. 1927)

137
Q

MEN1 tumor suppressor gene is found on what chromosome?

A

Long arm of chromosome 11q13

p. 1928

138
Q

What is the first step in the evaluation for ZES?

A

Fasting gastrin level

p. 1928

139
Q

Fasting gastrin level to diagnose/suspect gastrinoma

A

> 150-200 pg/ml

p. 1928

140
Q

Before testing for fasting gastrin levels to diagnose gastrinoma/ZES, PPIs should be discontinued at least how many days?

A

7 days

p. 1928

141
Q

What is considered to be pathognomonic of ZES?

A

Basal acid output (BAO) >15 meq/h

p. 1928

142
Q

The most sensitive and specific gastrin provocative test for the diagnosis of gastrinoma

A

Secretin study

p. 1928

143
Q

Treatment of choice for ZES

A

Proton pump inhibitors

p. 1929

144
Q

Favorable prognostic indicators for ZES

A 
Primary duodenal wall tumors
Isolated lymph node tumor
Presence of MEN1
Undetectable tumor upon surgical exploration
(p. 1929)
145
Q

Poor prognostic indicators for ZES

A 
Shorter disease duration
Higher gastrin levels (>10,000 pg/ml)
Large pancreatic primary tumors (>3cm)
Metastatic disease to lymph nodes, liver, and bone
Cushing' syndrome
Rapid growth of hepatic metastasis
(p. 1929)
146
Q

Most common presentation of Stress-related mucosal injury

A

GI bleeding

p. 1929

147
Q

Risk factors for bleeding in stress-related mucosal injury

A

Respiratory failure requiring mechanical ventilation
Coagulopathy
(p. 1929)

148
Q

Stress ulcer after head trauma

A

Cushing’s ulcer

p. 1930

149
Q

Stress ulcer after severe burns

A

Curling’s ulcer

p. 1930

150
Q

Sucralfate use in endotracheal intubated patients has been associated with ___.

A

Aspiration pneumonia

p. 1930

151
Q

Treatment of choice for stress ulcer prophylaxis

A

Proton pump inhibitors

p. 1930

152
Q

Definition: histologically documented inflammation of the gastric mucosa

A

Gastritis

p. 1930

153
Q

Three phases of gastritis

A

Superficial gastritis
Strophic gastritis
Gastric atrophy
(p. 1930)

154
Q

Phase of gastritis wherein inflammatory changes are limited to the lamina proprietary of the surface mucosa, with edema and cellular infiltrates separating intact gastric glands

A

Superficial gastritis

p. 1930

155
Q

Phase of gastritis wherein inflammatory infiltrates extend deeper into the mucosa, with progressive distortion and destruction of the glands

A

Atrophic gastritis

p. 1930

156
Q

Phase of gastritis wherein glandular structures are lost and there is paucity of inflammatory infiltrates

A

Gastric atrophy

p. 1930

157
Q

Type of gastritis that spares the antrum

A

Type A gastritis

p. 1931

158
Q

Type of gastritis which is also known as autoimmune gastritis

A

Type A gastritis

p. 1931

159
Q

This type of gastritis has been associated with pernicious anemia

A

Type A gastritis

p. 1931

160
Q

Higher incidence of these specific histocompatibility haplotypes have been noted in Type A gastritis

A

HLA-B8
HLA-DR3
(p. 1931)

161
Q

Type of gastritis which is antral-predominant

A

Type B gastritis

p. 1931

162
Q

More common form of gastritis (Type A / B?)

A

Type B gastritis

p. 1931

163
Q

Type of gastritis associated with H.pylori infection

A

Type B gastritis

p. 1931

164
Q

What type of disease/condition is associated with long term use of PPIs in older women?

A

Hip fracture

p. 1921

165
Q

Type of gastritis: mucosal lesion of unknown etiology that has a pseudotumoral endoscopic appearance

A

Russell body gastritis (RBG)

p. 1932

166
Q

Russell body gastritis is histologically defined by the presence of numerous plasma cells containing Russell bodies that express ____ and ____ light chains.

A

Kappa and lambda

p. 1932

167
Q

Very rare gastropathy characterized by large, tortuous mucosal folds

A

Menetrier’s Disease

p. 1932

168
Q

Often etiology of Menetrier’s Disease in children

A

CMV

p. 1932

169
Q

First line treatment for Menetrier’s Disease

A

Cetuximab

p. 1932

170
Q

Three types of intestinal ischemia based on etiology

A

Arterioocclusive mesenteric ischemia
Non-occlusive mesenteric ischemia
Mesenteric venous thrombosis
(p. 1978)

171
Q

Risk factors for arterioocclusive mesenteric ischemia

A 
Atrial fibrillation
Recent myocardial infarction
Valvular heart disease
Recent cardiac or vascular catheterization
(p. 1979)
172
Q

Type of intestinal ischemia which is the most prevalent gastrointestinal disease complicating cardiovascular surgery

A

Non-occlusive mesenteric ischemia

p. 1979

173
Q

Type of intestinal ischemia associated with the presence of a hypercoagulable state (protein C/S deficiency, anti-thrombin III deficiency, polycythemia vera, etc)

A

Mesenteric venous thrombosis

p. 1979

174
Q

What are Griffith’s point and Sudeck’s point?

A

Most common locations for colonic ischemia

p. 1979

175
Q

What are the two most common locations for colonic ischemia?

A

Griffith’s point and Sudeck’s point

p. 1979

176
Q

Splanchnic circulation can receive up to how many percent of the cardiac output?

A

30%

p. 1979

177
Q

In occlusive mesenteric ischemia, where do emboli preferentially lodge?

A

Superior mesenteric artery, distal to the origin of the middle colic artery
(p. 1979)

178
Q

Intestinal ischemia that is disproportionate mesenteric vasoconstriction (vasospasm) in response to a severe physiologic stress (e.g. Shock)

A

Non-occlusive ischemia

p. 1979

179
Q

What disease/condition presents with severe, acute, nonremitting abdominal pain that is out of proportion to the physical findings?

A

Acute mesenteric ischemia

p. 1979

180
Q

Plain abdominal film findings for mesenteric ischemia

A

Evidence of free peritoneal air indicating a perforated viscus
“Thumbprinting” - bowel wall edema
Pneumatosis intestinalis - air seen within the bowel wall when ischemia progresses
(p. 1979)

181
Q

Air seen within the bowel wall in plain abdominal Xray of intestinal ischemia

A 
Pneumatosis intestinalis
(p. 1979)
182
Q

Screening test for mesenteric ischemia

A

Mesenteric duplex scan

p. 1979

183
Q

Highly sensitive test for intestinal ischemia

A

Dynamic CT angiography

p. 1979

184
Q

What is the gold standard for the diagnosis of acute arterial occlusive disease?

A

Angiography

p. 1980

185
Q

What is the management for acute arterial occlusive disease?

A

Laparotomy

p. 1980

186
Q

Markers for intestinal ischemia

A 
D-dimer
Glutathione S-transferase
Platelet-activating factor (PAF)
Mucosal pH monitoring
(p. 1980)
187
Q

On colonoscopy, MILD ischemic colitis is seen as?

A

Minimal mucosal erythema

p. 1980

188
Q

On colonoscopy, MODERATE ischemic colitis is seen as?

A

Pale mucosal ulcerations and evidence of extension to the muscular layer of the bowel wall
(p. 1980)

189
Q

On colonoscopy, SEVERE ischemic colitis is seen as?

A

Severe ulcerations resulting in black or green discoloration of the mucosa, consistent with full-thickness bowel wall necrosis
(p. 1980)

190
Q

Degree of reversibility of mild ischemic colitis

A

100% reversible

p. 1980

191
Q

Degree of reversibility of moderate ischemic colitis

A

50% reversible

p. 1980

192
Q

Degree of reversibility of severe ischemic colitis

A

Irreversible

p. 1980

193
Q

Diagnostic modality for mesenteric thrombosis

A

Abdominal Spiral CT with oral and IV contrast

p. 1980

194
Q

Among the types of intestinal ischemia/disorders, which has the best prognosis?

A

Mesenteric venous insufficiency

p. 1981

195
Q

What disease/condition presents as abdominal cramping and pain following ingestion of a meal, and often shows a malnourished patient with an abdominal bruit?

A

Chronic intestinal ischemia

p. 1981

196
Q

In equivocal cases after revascularization of intestinal ischemia, what can be administered to observe the pattern of bowel reperfusion?

A

1 gram of IV sodium fluorescein

p. 1981

197
Q

This occurs when the bowel twists on its mesenteric axis

A

Volvulus

p. 1982

198
Q

What area is most commonly affected in volvulus?

A

Sigmoid colon

p. 1982

199
Q

Risk factors for volvulus

A 
Institutionalization
Presence of neuropsychiatric conditions requiring psychotropic medication
Chronic constipation
Aging
(p. 1982)
200
Q

Also known as ileum and pseudo-obstruction

A 
Functional obstruction
(p. 1982)
201
Q

This is the condition in which dysmotility prevents intestinal contents from being propelled dismally but no mechanical blockage exists

A 
Functional obstruction
(p. 1982)
202
Q

Pseudo-obstruction of the colon

A

Ogilvie’s syndrome

p. 1982

203
Q

What is Ogilvie’s syndrome?

A

Pseudo-obstruction of the colon

p. 1982

204
Q

Epithelial necrosis can be identified within how many hours of intestinal obstruction?

A

Within 12 hours

p. 1982

205
Q

In intestinal obstruction, the most commonly cultured intraluminal organisms are?

A

E. coli
Streptococcus feacalis
Klebsiella
(p. 1982)

206
Q

This results when the proximal and distal openings of a given bowel segment are both occluded

A

Closed-loop obstruction

p. 1982

207
Q

What is the most common precursor for bowel strangulation?

A

Closed-loop obstruction

p. 1982

208
Q

The risk for cecal perforation is greatest when the cecal diameter exceeds ____.

A

12 cm

p. 1982

209
Q

Cardinal signs of intestinal obstruction

A 
Colicky abdominal pain
Abdominal distention
Eyes is
Obstipation
(p. 1983)
210
Q

Patients with more proximal intestinal obstruction commonly present with less abdominal distention but more pronounced ___.

A

Vomiting

p. 1983

211
Q

Classical findings in plain abdominal Xray of small bowel obstruction

A

“Staircasing” pattern of dilated air and fluid-filled small bowel loops >2.5 cm in diameter
Little or no air seen in the colon
(p. 1984)

212
Q

“Coffee-bean” shaped dilated shadow in plain abdominal Xray may be seen in what condition?

A

Volvulus

p. 1984

213
Q

Most commonly used imaging modality for intestinal obstruction

A

CT scan

p. 1984

214
Q

CT scan findings of “bird’s beak”, a “c-loop”, or “whorl”

A

Colonic volvulus

p. 1984

215
Q

This diagnostic modality is generally contraindicated in patients with firm evidence of complete or high grade bowel obstruction

A

Barium studies

p. 1984

216
Q

An acetylcholinesterase inhibitor which can stimulate colonic motility

A

Neostigmine

p. 1985

217
Q

Intravenous administration of this drug induces defamation and flats within 10 minutes in majority of patients with Ogilvie’s disease

A

Neostigmine

p. 1985

218
Q

Treatment for cecal volvulus

A

Laparotomy or laparoscopic correction

p. 1985

219
Q

Treatment for sigmoid volvulus

A

Decompression using a flexible tube through a rigid proctoscope or sigmoidoscope
(p. 1985)

220
Q

At operation, what is a defining feature of bowel obstruction?

A

Dilation proximal to the site of blockage with distal collapse
(p. 1985)

221
Q

Where is the most common site of intestinal obstruction in patients with gallstone “ileus”?

A

Ileum (60%)

p. 1985

222
Q

In gallstone ileus, the gallstone enters the intestinal tract most often via what/where?

A

Cholecystoduodenal fistula

p. 1985

223
Q

Early postoperative mechanical bowel obstruction occurs within the first ___ weeks of operation.

A

6 weeks

p. 1985

224
Q

Most common emergency general surgical disease affecting the abdomen

A

Appendicitis

p. 1985

225
Q

Appendicitis is more common in men with a male-to-female ratio of ___.

A
  1. 4:1

p. 1985

226
Q

Most important cause of excess morbidity and mortality in Appendicitis

A

Perforation

p. 1985

227
Q

Believed to be an important step in the development of appendicitis

A

Obstruction of the appendiceal lumen

p. 1986

228
Q

Patients with appendicitis who have had symptoms for more than ___ hours are more likely to perforate.

A

48

p. 1986

229
Q

True or false:
Appendicitis should be included in the differential diagnosis of abdominal pain for every patient in any age group unless certain that the organ has been previously removed.

A

True

p. 1986

230
Q

True or false: In appendicitis, abdominal pain is experienced first before nausea.

A

True

p. 1987

231
Q

True or false: In appendicitis, nausea comes first before abdominal pain.

A

False

p. 1987

232
Q

True or false: In gastroenteritis, nausea comes first before abdominal pain.

A

True

p. 1987

233
Q

The absence of this symptom should question the diagnosis of appendicitis

A

Anorexia

p. 1987

234
Q

___ appendicitis are more likely to present with dysuria, urinary frequency, diarrhea, or tenesmus.

A

Pelvic

p. 1987

235
Q

Gynecologic diseases/conditions that may mimic appendicitis

A

Pelvic inflammatory disease
Ectopic pregnancy
Ovarian torsion
(p. 1987)

236
Q

In appendicitis, maximal tenderness is classically identified where?

A

RLQ at or near the McBurney’s point

p. 1987

237
Q

Where is McBurney’s point?

A

1/3 of the way along a long originating at the anterior iliac spine running to the umbilicus
(p. 1987)

238
Q

Gentle pressure in the LLQ of the abdomen may elicit pain in the RLQ

A

Rovsing’s sign

p. 1987

239
Q

What is Rovsing’s sign?

A

Gentle pressure in the LLQ of the abdomen may elicit pain in the RLQ if the appendix is located there
(p. 1987)

240
Q

Most common presenting symptom of appendicitis?

A 
Abdominal pain (>95%)
(p. 1987, Table 356-2)
241
Q

What is obturator sign?

A

Internal rotation of the hip causes pain, suggesting the possibility of an inflamed appendix located in the pelvis
(p. 1987)

242
Q

What does a positive obturator sign mean?

A

Suggests the possibility of an inflamed appendix located in the pelvis
(p. 1987, Table 356-4)

243
Q

What is iliopsoas sign?

A

Extending the right hip causes pain alon posterolateral back and hip, suggesting retrocecal appendicitis
(p. 1987, Table 356-4)

244
Q

What does a positive iliopsoas sign mean?

A

Suggests retrocecal appendicitis

p. 1987, Table 356-4

245
Q

Ultrasound findings suggesting the presence of appendicitis

A

Wall thickening
Increased appendiceal diameter
Presence of free fluid
(p. 1988)

246
Q

Sensitivity and specificity of CT scan for diagnosing appendicitis

A

94 and 95%

p. 1988

247
Q

CT scan findings for appendicitis

A

Dilatation >6 mm with wall thickening
Lumen that does not fill with enteric contrast
Fatty tissue stranding or air surrounding the appendix
(p. 1988)

248
Q

What is the most common extrauterine general surgical emergency observed during pregnancy?

A

Appendicitis

p. 1988

249
Q

Why is diagnosing appendicitis difficult in pregnant women?

A

As the uterus enlarges, the appendix may be pushed higher along the right flank even to the RUQ
(p. 1988)

250
Q

Fetal mortality rate in pregnant women with perforated appendicitis

A

20% or 4x greater

p. 1988

251
Q

What is the appropriate management in patients with appendicitis presenting with a mass (representing a phlegmon or abscess)?

A 
Broad-spectrum antibiotics
Drainage if abscess >3 cm in diameter
Parenteral fluids
Bowel rest
(p. 1988)
252
Q

In patients with appendicitis presenting with a mass (representing phlegmon or abscess), when can the appendix be safely removed?

A

6-12 weeks later (when the inflammation has diminished)

p. 1988

253
Q

What is the most common postoperative complications of appendicitis?

A

Fever
Leukocytosis
(p. 1988)

254
Q

What are the cardinal signs and symptoms of peritonitis?

A

Acute severe abdominal pain with tenderness and fever

p. 1989

255
Q

Type of peritonitis which is commonly caused by the abnormal presence of physiologic fluids (e.g. Gastric juice, bile, pancreatic enzymes, blood, urine)

A

Aseptic peritonitis

p. 1989

256
Q

What forms the common bile duct?

A

Common hepatic duct and cystic duct

p. 2075

257
Q

Common bile duct enters the duodenum through the ___.

A

Ampulla of Vater

p. 2075

258
Q

The total daily basal secretion of hepatic bile is ___.

A

500-600 ml

p. 2075

259
Q

What are the three important mechanisms in regulating bile flow?

A

1) Active transport of bile acids from hepatocytes into the bile canaliculi
2) Active transport of other organic anions
3) Cholangiocellular secretion
(p. 2075)

260
Q

This is an aminophospholipid transferase “flippase” essential for maintaining the lipid asymmetry of the canalicular membrane

A

F1C1

p. 2075

261
Q

This is seen to be defective in progressive familial intrahepatic cholestasis type 1 (PFIC1) and benign recurrent intrahepatic cholestasis type 1 (BRIC1)

A

F1C1

p. 2076

262
Q

This pump is seen to be defective in progressive familial intrahepatic cholestasis type 2 (PFIC2) and benign recurrent intrahepatic cholestasis type 2 (BRIC2)

A

Bile salt export pump (BSEP)

p. 2076

263
Q

Mutations of ___ cause the Dubin-Johnson syndrome

A

An ionic conjugate export pump (MRP2)

p. 2076

264
Q

Defect in ___ results in progressive familial intrahepatic cholestasis type 3 (PFIC3)

A

Phospholipid export pump (MDR3)

p. 2076

265
Q

This pump is seen to be defective in sitosterolemia

A

Canalicular cholesterol and phytoestrogens transporter (ABCG5/G8)
(p. 2076)

266
Q

This pump is seen to be defective in cystic fibrosis

A

Cystic fibrosis transmembrane regulator (CFTR)

p. 2076

267
Q

What are the primary bile acids?

A

Cholic acid
Chenodeoxycholic acid (CDCA)
(p. 2076)

268
Q

The primary bile acids are conjugated with what amino acid/s before being secreted into the bile?

A

Glycine OR taurine

p. 2076

269
Q

What are the secondary bile acids?

A

Deoxycholate
Litocholate
Ursodeoxycholic acid (UDCA)
(p. 2076)

270
Q

Micelles are molecular aggregates of ___.

A

Bile acids

p. 2076

271
Q

Unconjugated bile acids are absorbed along the entire gut by ___.

A

Passive diffusion

p. 2076

272
Q

The normal bile acid pool size is ___.

A

2-4 grams

p. 2076

273
Q

Normally, how many times does the bile acid pool circulate?

A

5-10 times

p. 2076

274
Q

Bile acids in the intestine release what growth factor into the circulation, which when transported to the liver suppresses synthesis of bile acids from cholesterol and promotes gallbladder relaxation?

A

Fibroblast growth factor 19 (FGF19)

p. 2076

275
Q

Fibroblast growth factor 19 (FGF19) released by bile acids in the intestine functions to:

A

1) Suppress synthesis of bile acids from cholesterol by inhibiting CYP7A1
2) Promotes gallbladder relaxation
(p. 2076)

276
Q

What receptor is a bile acid sensor that also represses bile acid synthesis?

A

Farnesoid X receptor (FXR)

p. 2076

277
Q

ABC65/G8 is upregulated by which receptor, which is also an oxysterol sensor?

A

Liver X receptor (LXR)

p. 2076

278
Q

Tonic contraction of the Sphincter of Oddi functions to:

A

1) Prevent reflux of duodenal contents into the pancreatic and bile ducts
2) Promote filling of the gallbladder
(p. 2076)

279
Q

WHich hormone is released from the duodenal mucosa in response to the ingestion of fats and amino acids?

A

Cholecystokinin (CCK)

p. 2076

280
Q

What is/are the function/s of CCK?

A

1) Produces powerful contraction of the gallbladder
2) Decrease resistance of the sphincter of Oddi
3) Enhance flow of biliary contents into the duodenum
(p. 2076)

281
Q

The normal capacity of the gallbladder is ___ ml of bile.

A

30

p. 2076

282
Q

Clinically innocuous entity in which a partial or complete septum (or fold) separates the fundus from the body

A

Phrygian cap

p. 2076

283
Q

This condition predisposes to acute torsion, volvulus, or herniation of the gallbladder

A

Floating gallbladder

p. 2076

284
Q

Type of gallstone that account for more than 90% of all gallstones, which usually contain >50% cholesterol monohydrate plus an admixture of calcium salts, bile pigments, proteins, and fatty acids

A

Cholesterol stones

p. 2076

285
Q

Type of gallstone that is composed primarily of calcium bilirubinate

A

Pigment stones

p. 2076

286
Q

Type of gallstone that is classified into “black” and “brown” types

A

Pigment stones

p. 2076

287
Q

What is the rate limiting enzyme of hepatic cholesterol synthesis?

A

HMG-CoA reductase

p. 2077

288
Q

True or false: In patients without gallstones, dietary cholesterol increases biliary cholesterol secretion.

A

False, only occurs in patients with gallstones

p. 2077

289
Q

What gene mutation results in a deficiency of the enzyme cholesterol 7-hydroxylase (initial step in cholesterol catabolism and bile acid synthesis)?

A

CYP7A1 gene

p. 2077

290
Q

What gene mutation can cause defective phospholipid secretion into bile, thus resulting in cholesterol supersaturation of bile?

A

MDR3 gene

p. 2077

291
Q

Where do cholesterol monohydrate crystal nucleation and crystal growth probably occur?

A

Mucin gel layer

p. 2077

292
Q

What do you call a thick, mucous material that reveals lecithin-cholesterol liquid crystals, cholesterol monohydrate crystals, calcium bilirubinate, and mucin gels upon microscopic examination?

A

Binary sludge

p. 2077

293
Q

What typically forms a crescent-like layer in the most dependent portion of the gallbladder recognized by the characteristic echoes on UTZ?

A

Biliary sludge

p. 2077

294
Q

The presence of biliary sludge implies what two abnormalities?

A

1) The normal balance between gallbladder mucin secretion and elimination has become deranged
2) Nucleation of biliary salutes has occurred
(p. 2077)

295
Q

True or false: Pregnancy is associated with biliary sludge formation.

A

True

p. 2078

296
Q

True or false: Rapid weight loss reduction through very-low calorie diet can cause biliary sludge.

A

True

p. 2078

297
Q

What are the two key changes during pregnancy that contribute to a “cholelithogenic state”?

A

1) Marked increase in cholesterol saturation of bile during the 3rd trimester
2) Sluggish gallbladder contraction in response to a standard meal
(p. 2078)

298
Q

Cholesterol gallstone disease occurs because of what 3 mechanisms?

A

1) Bile supersaturation with cholesterol
2) Nucleation of cholesterol monohydrate with subsequent crystal retention and stone growth
3) Abnormal gallbladder motor function with delayed emptying and stasis
(p. 2078)

299
Q

Gallstones composed of either pure bilirubinate or polymer-like complexes with calcium and mucin glycoproteins

A

Black pigment stones

p. 2078

300
Q

Type of pigment stone that is more common in patients who have chronic hemolytic states, liver cirrhosis, Gilbert’s syndrome, or cystic fibrosis

A

Black pigment stones

p. 2078

301
Q

Gallbladder stones in patients with ileal diseases, ileal resection, or ileal bypass are generally what type of pigment stones?

A

Black pigment stones

p. 2078

302
Q

What type of pigment stone is composed of calcium salts of unconjugated bilirubin with varying amounts of cholesterol and protein?

A

Brown pigment stones

p. 2078

303
Q

This type of pigment stone is caused by the presence of increased amounts of unconjugated, insoluble bilirubin in bile that precipitate to form stones

A

Brown pigment stones

p. 2078

304
Q

Deconjugation of an excess of soluble bilirubin mono- and diglucuronides may occur by spontaneous hydrolysis OR may be mediated by what enzyme?

A

Beta-glucuronidase

p. 2078

305
Q

What imaging test is very accurate in the identification of cholelithiasis (has replaced oral cholecystography)?

A

Ultrasound of the gallbladder

p. 2078

306
Q

In UTZ of the gallbladder, stones as small as ____ in diameter may be confidently identified

A
  1. 5 mm

p. 2078

307
Q

In UTZ of the gallbladder, what does biliary sludge look like?

A

Material of low echogenic activity that typically forms a layer in the most dependent portion of the gallbladder
(p. 2078)

308
Q

In UTZ of the gallbladder, how do you differentiate biliary sludge from gallstones?

A

Biliary sludge fails to produce acoustic shadowing

p. 2078

309
Q

True or false: Ultrasound of the gallbladder can be used to assess the emptying function of the gallbladder

A

True

p. 2078

310
Q

UTZ criteria to diagnose gallstones

A

Acoustic shadowing of opacities that are within the gallbladder lumen and that change with the patient’s position (by gravity)
(p. 2078)

311
Q

Plain abdominal film in cholelithiasis may be used in diagnosing what gallbladder/bile conditions?

A 
Emphysematous cholecystitis
Porcelain gallbladder
Limey bile
Gallstone ileus
(p. 2078)
312
Q

Imaging test that has historically been a useful procedure for the diagnosis of gallstones but is now regarded obsolete

A

Oral cholecystography

p. 2078

313
Q

Imaging/diagnostic test used for accurate identification of cystic duct obstruction with simultaneous assessment of bile ducts

A 
Radioisotope scans (HIDA, DIDA, DISIDA, etc)
(Pp. 2078, 2079)
314
Q

What is the most specific and characteristic symptom of gallstone disease?

A

Biliary colic

p. 2079

315
Q

True or false: Biliary colic is frequently nocturnal

A

True

p. 2080

316
Q

True or false: Up to 80% of persons with a symptomatic gallstones remain asymptomatic over up to 25 years

A

True

p. 2080

317
Q

The recommendation for cholecystectomy in a patient with gallstones should probably be based on assessment of what factors (three)?

A

1) Presence of symptoms that are frequent enough or severe enough to interfere with patient’s general routine
2) Presence of a prior complication of gallstone disease
3) Presence of an underlying condition predisposing the patient to increased risk of gallstone complications
(p. 2080)

318
Q

Prophylactic cholecystectomy may be considered in what conditions?

A

1) Patients with very large gallstones (>3cm in diameter)
2) Patients with gallstones.in a congenitally anomalous gallbladder
(p. 2080)

319
Q

What is the gold standard for treating symptomatic cholelithiasis?

A

Laparoscopic cholecystectomy

p. 2080

320
Q

In gallstone disease, UDCA may be used in radiolucent stones smaller than ____ in diameter.

A

5 mm

p. 2080

321
Q

Dose of UDCA

A

10-15 mg/kg/day

p. 2080

322
Q

True or false: Pigment stones are responsive to UDCA therapy

A

False

p. 2080

323
Q

True or false: Patients with cholesterol gallstone disease who develop recurrent choledocholithiasis after cholecystectomy should be on long-term treatment with UDCA

A

True

p. 2080

Internal Medicine (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions