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
2
Q
Pyloric glands are found where?
A
Antrum
p. 1911
3
Q
The parietal cell is also known as?
A
oxyntic cell
p. 1911
4
Q
The parietal cell is usually found where?
A
Neck / isthmus / oxyntic gland
p. 1911
5
Q
The gastric epithelial lining consists of rugae that contain what?
A
Gastric pits
p. 1911
6
Q
Where specifically does acid secretion occur?
A
Apical canalicular surface
p. 1912
7
Q
First line of defense in the mucosal defense system?
A
Mucus-bicarbonate-phospholipid layer
p. 1912
8
Q
Mucus is composed of what?
A
Water (95%) and mixture of phospholipids and glycoproteins (mucin)
(p. 1912)
9
Q
Function of mucus
A
Impedes diffusion of ions and molecules (e.g. Pepsin)
p. 1912
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
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)
12
Q
What is restitution?
A
When gastric epithelial cells bordering a site of injury can migrate to restore a damaged region
(p. 1912)
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)
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)
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)
16
Q
COX-1 is expressed what tissues?
A
Stomach, platelets, kidneys, endothelial cells
p. 1912
17
Q
COX-2 is expressed in what cells?
A
Macrophages, leukocytes, fibroblasts, synovial cells
p. 1912
18
Q
Selective COX-2 inhibitors with adverse effect of myocardial infarction, therefore was removed from the market?
A
Valdecoxib and Rofecoxib
p. 1912
19
Q
What are the two principal gastric secretory products capable of inducing mucosal injury?
A
Hydrochloric acid and pepsinogen
p. 1912
20
Q
HCl and pepsinogen play a role in the absorption of what nutrients/vitamins?
A
Iron, calcium, magnesium, vitamin B12
p. 1912
21
Q
Basal acid production occurs in a circadian pattern with the highest levels occurring during the _____.
A
Night
p. 1912
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)
23
Q
Stimulated gastric secretion occurs primarily in three phases, namely:
A
Cephalic
Gastric
Intestinal
(p. 1912)
24
Q
The GI hormone somatostatin is release from what cells?
A
Endocrine cells found in the gastric mucosa (D cells)
p. 1912
25
Somatostatin is released in response to?
HCl
| p. 1912
26
How can somatostatin inhibit acid production directly and indirectly?
Directly via the parietal cell
Indirectly by decreased histamine release from ECL cells and gastrin release from G cells
(p. 1912)
27
Hormone that may increase gastric acid secretion through stimulation of histamine release from ECL cells
Ghrelin
| Pp. 1912-1913
28
Ghrelin is expressed in what cell?
Gr cells in the stomach
| p. 1912
29
Which cell secretes intrinsic factor (IF) and IL-11?
Parietal cell
| p. 1913
30
The parietal cell expresses receptors for several stimulants of acid secretion, which includes:
Histamine (H2)
Gastrin (cholecystokinin B / gastrin receptor)
Acetylcholine (muscarinic, M3)
(p. 1913)
31
Histamine stimulates gastric acid secretion indirectly by?
Activating the histamine H3 receptor on D cells --> inhibits somatostatin release
(p. 1913)
32
Active catalytic site of the enzyme H+K+-ATPase is found within the ___ subunit
Alpha
| p. 1913
33
Where are chief cells located?
Primarily in the gastric fundus
| p. 1914
34
What cell synthesizes and secretes pepsinogen and where is it found?
Chief cell - gastric fundus
| p. 1914
35
Pepsin activity is significantly diminished at a pH of?
4
| p. 1914
36
Pepsin activity is irreversibly inactivated and denatured at a pH of?
Greater than or equal to 7
| p. 1914
37
Ulcers are defined as?
Breaks in the mucosal surface >5 mm in size, with depth to the submucosa
(p. 1914)
38
What are the two most common risk factors for PUD?
Helicobacter pylori
NSAIDs
(p. 1914)
39
___ ulcers tend to occur later in life with a peak incidence in the sixth decade of life.
Gastric
| p. 1914
40
Duodenal ulcers occur most often in which part of the duodenum?
```
First part (>95%)
(p. 1914)
```
41
Which type of ulcer should be biopsies upon discovery?
Gastric ulcers
| p. 1915
42
Where are benign gastric ulcers most often found?
Distal to the junction between the antrum and the acid secretory mucosa
(p. 1915)
43
How many types of gastric ulcer are there?
4
| p. 1915
44
Which type of gastric ulcer occur in the gastric body and tend to be associated with low gastric acid production?
Type I
| p. 1915
45
Which type of gastric ulcer occur in the antrum and gastric acid can vary from low to normal?
Type II
| p. 1915
46
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?
Type III
| p. 1915
47
Which gastric ulcer is found in the cardio and is associated with low gastric acid production?
Type IV
| p. 1915
48
Where is a Type I gastric ulcer located?
Gastric body
| p. 1915
49
Where is a Type II gastric ulcer located?
Antrum
| p. 1915
50
Where is a Type III gastric ulcer located?
Within 3 cm of the pylorus
| p. 1915
51
Where is a Type IV gastric ulcer located?
Cardia
| p. 1915
52
Which type of gastric ulcer is the only one associated with high gastric acid secretion?
Type III
| p. 1915
53
H. Pylori plays a role in the development of which conditions?
Peptic Ulcer Disease (PUD)
Gastric mucosa-associated lymphoid tissue (MALT) lymphoma
Gastric adenocarcinoma
(p. 1915)
54
H. Pylori was initially called?
Campylobacter pyloridis
| p. 1915
55
Two factors that predispose to higher colonization rates of H. Pylori
Poor socioeconomic status
Less education
(p. 1915)
56
Risk factors for H. Pylori infection
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)
57
Transmission of H. Pylori
Oral-oral
Fecal-oral
(p. 1915)
58
H. Pylori is present in how many % of individuals with gastric ulcers?
30-60%
| p. 1915
59
H. Pylori is present in how many % of individuals with duodenal ulcers?
50-70%
| p. 1915
60
Which specific region of the bacterial genome encodes the virulence factors Cag A and pic B?
cag-PAI
| p. 1915
61
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?
Vac A
| p. 1915
62
H. Pylori strains that are ____ positive are associated with higher risk of PUD, premalignant gastric lesions, and gastric cancer
Cag-PAI
| p. 1915
63
Which enzyme allows the H. Pylori bacteria to reside in the acidic stomach?
Urease
| p. 1916
64
How does urease allow the H. Pylori bacteria to reside in the stomach?
It generates NH3, which can damage epithelial cells
| p. 1916
65
Elevated concentrations of multiple cytokines are found in the gastric epithelium of H. Pylori-infected individuals, namely:
```
IL-1a/B
IL-2
IL-6
IL-8
TNF-a
IFN-Y
(p. 1916)
```
66
The presence of antral-predominant gastritis is associated with ___ ulcer.
Duodenal
| p. 1916
67
Gastritis involving the corpus predisposes to development of ___ ulcer.
Gastric
| p. 1916
68
Risk factors for NSAID-induced ulcer
```
Advanced age
History of ulcer
Use of glucocorticoids, high-dose NSAIDs, multiple NSAIDs
Use of anticoagulants/clopidogrel
Serious multi system disease
(p. 1917)
```
69
Chronic disorders shown to have a STRONG association with PUD
```
Advanced age
Chronic pulmonary disease
Chronic renal failure
Cirrhosis
Nephrolithiasis
A1-antitrypsin deficiency
Systemic mastectomies
(p. 1917)
```
70
Disorders with a POSSIBLE association with PUD
```
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)
```
71
Typical abdominal pain pattern of duodenal ulcer
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)
72
Most discriminating symptom of duodenal ulcer
Pain that awakens the patient from sleep (between 12mn-3am)
| p. 1918
73
In PUD, elderly patients are less likely to have abdominal pain and may instead present as?
Bleeding or perforation
| p. 1918
74
What is the most frequent PE finding in patients with gastric/duodenal ulcers?
Epigastric tenderness
| p. 1918
75
PE of patient with gastric/duodenal ulcer: A severely tender, board-like abdomen suggests?
Perforation
76
Presence of succussion splash suggests?
Gastric outlet obstruction
| p. 1918
77
What is the most common complication observed in PUD?
GI Bleeding
| p. 1918
78
GI bleeding as a complication of PUD occurs in how many percent of individuals?
15%
| p. 1918
79
What is the second most common complication of PUD?
Perforation
| p. 1918
80
Perforation as a complication of PUD occurs in how many percent of individuals?
6-7%
| p. 1918
81
___ is a form of perforation in which the ulcer bed tunnels into an adjacent organ.
Penetration
| p. 1918
82
Duodenal ulcers tend to penetrate where?
Posteriorly into the pancreas
| p. 1918
83
Gastric ulcers tend to penetrate where?
Left hepatic lobe
| p. 1918
84
What is the least common PUD-related complication?
Gastric outlet obstruction
| p. 1918
85
Gastric outlet obstruction as a complication of PUD occur in how many percent of individuals?
1-2%
| p. 1918
86
This refers to a group of heterogenous disorders typified by upper abdominal pain without the presence of an ulcer
NUD / functional dyspepsia / essential dyspepsia
| p. 1918
87
Appearance of a duodenal ulcer
Well-demarcated crater, most often seen in the bulb
| p. 1919
88
Appearance of a benign gastric ulcer
Discrete crater with radiating mucosal folds originating from the ulcer margin
(p. 1919)
89
Ulcers ___ in size or associated with a mass are more often malignant.
>3 cm
| p. 1919
90
What is the most sensitive and specific approach for examining the upper GI tract (for PUD)
Endoscopy
| p. 1919
91
Specialized testing may be needed to be done in individuals with complicated or refractory PUD. Examples of which are:
Serum gastrin
Gastric acid analysis
Sham feeding
(p. 1919)
92
Infectious causes of ulcers not caused by H.pylori or NSAIDs
Cytomegalovirus
Herpes simplex virus
Helicobacter heilmannii
(p. 1918, Table 348-1)
93
Drug/toxic causes of ulcers not caused by H.pylori and NSAIDs
```
Bisphosphonates
Chemotherapy
Clopidogrel
Crack cocaine
Glucocorticoids (when combined with NSAIDs)
Mycophenolate mofetil
Potassium chloride
(p. 1918, Table 348-1)
```
94
Invasive tests for detection of H.pylori
Rapid urease
Histology
Culture
(p. 1920)
95
Non-invasive tests for detection of H.pylori
Serology
Urea breath test
Stool antigen
(p. 1920, Table 348-2)
96
Mainstay of treatment of PUD (non-pharmacological)
Eradication of H.pylori
Prevention of NSIAID-induced disease
(p. 1919)
97
Side effect of aluminum hydroxide
Constipation
Phosphate depletion
(p. 1920)
98
Side effect of magnesium hydroxide
Loose stools
| p. 1920
99
Magnesium-containing preparation (antacid) should not be used in chronic renal failure patients because?
Possible hypermagnesemia
Chronic neurotoxicity (due to aluminum)
(p. 1920)
100
Milk-alkali syndrome is caused by?
Long term use of calcium carbonate
| p. 1920
101
What is milk-alkali syndrome?
```
Hypercalcemia
Hyperphosphatemia
Possible renal calcinosis
Progression to renal insufficiency
(p. 1920)
```
102
First H2 receptor antagonist used for treatment of acid peptic disorders
Cimetidine
| p. 1920
103
Which H2 receptor antagonist has a weak antiandrogenic effect resulting in reversible gynecomastia and impotence?
Cimetidine
| p. 1920
104
Which H2 receptor antagonists can bind to hepatic cytochrome P450?
Cimetidine
Ranitidine
(p. 1920)
105
Substituted benzimidazole derivatives that covalently bind and irreversibly inhibit H+,K+-ATPase
Proton pump inhibitors
106
Purposes of sodium bicarbonate in combination with PPIs:
1) Protect the Omeprazole from acid degradation
2) Promote rapid gastric alkalinization and subsequent proton pump activation
(p. 1920)
107
Half-life of PPIs
~18 hours
| p. 1921
108
Mechanism for rebound gastric hypersecretion after discontinuation of PPIs
Gastrin-induced hyperplasia and hyper trophy of histamine-secreting ECL cells
(p. 1921)
109
Long term acid suppression (esp. with PPIs) has been associated with a higher incidence of what conditions?
Community-acquired pneumonia
Community and hospital acquired Clostridium difficile-associated disease
(p. 1921)
110
PPI containing an imidazopyridine ring instead of a benzimidazole ring, which promotes irreversible proton pump inhibition
Tenatoprazole
| p. 1921
111
PPI that has a longer half-life and may be beneficial for inhibiting nocturnal acid secretion
Tenatoprazole
| p. 1921
112
Pharmacologic: complex sucrose salt in which the hydroxyl groups have been substituted by aluminum hydroxide and sulfate
Sucralfate
| p. 1921
113
Adverse effects of short term use of bismuth-containing compounds
Black stools
Constipation
Darkening of the tongue
(p. 1921)
114
Adverse effect of long term use of bismuth-containing compounds
Neurotoxicity
| p. 1921
115
The Maastricht IV/Florence Concensus Report recommends that eradication of H.pylori should be considered in the ff:
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)
116
Risk factors for gastric cancer
Heavy smoking
High exposure to dust, coal, quartz, cement
Work in the quarries
(p. 1922)
117
First triple regimen found effective against H.pylori
Bismuth, metronidazole, and tetracycline
| p. 1922
118
Failure of H.pylori eradication with triple therapy in a compliant patient is usually due to what?
Infection with a resistant organism
| p. 1923
119
What pharmacologic agent can heal gastric/duodenal ulcers independent of whether NSAIDs are discontinued?
PPIs
| p. 1923
120
This study demonstrated that the advantage of Celecoxib in preventing GI complications was offset when low-dose aspirin was used simultaneously
CLASS study
| p. 1923
121
Treatment for gastric/duodenal ulcer caused by H.pylori?
Triple therapy for 14 days followed by continued acid-suppressing drugs (H2 blocker or PPI) for a total of 4-6 weeks
(p. 1924)
122
Test of choice for documenting eradication of H.pylori
Stool antigen test OR urea breath test
| p. 1924
123
For gastric ulcer negative for neoplasm on initial endoscopy/biopsy, when should repeat endoscopy be done?
8-12 weeks
| p. 1924
124
When is a gastric ulcer considered to be refractory to therapy?
If it fails to heal after 12 weeks of therapy
| p. 1924
125
When is a duodenal ulcer considered to be refractory to therapy?
If it fails to heal after 8 weeks of therapy
| p. 1924
126
Signs and symptoms of EARLY dumping syndrome is due to what?
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)
127
LATE phase of dumping syndrome is due to what?
Hypoglycemia from excessive insulin release
| p. 1926
128
Dumping syndrome is most noticeable after meals rich in ___.
```
Simple carbohydrates (especially sucrose) and high osmolarity
(p. 1926)
```
129
Cornerstone of therapy for patients with dumping syndrome
Dietary modification
| p. 1926
130
Pathophysiology: Hypergastrinemia originating from an autonomous neoplasm
Zollinger-Ellison Syndrome
| p. 1927
131
Borders of the gastrinoma triangle
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
Most common clinical manifestation of ZES
Peptic ulcer
| p. 1927
133
Clinical situations that should create suspicion of gastrinoma
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
Second most common clinical manifestation of ZES
Diarrhea
| p. 1927
135
Gastrinomas can develop in the presence of what autosomal dominant disorder?
MEN 1 syndrome
| p. 1927
136
MEN 1 syndrome involves primarily what organ sites?
Parathyroid glands
Pancreas
Pituitary gland
(p. 1927)
137
MEN1 tumor suppressor gene is found on what chromosome?
Long arm of chromosome 11q13
| p. 1928
138
What is the first step in the evaluation for ZES?
Fasting gastrin level
| p. 1928
139
Fasting gastrin level to diagnose/suspect gastrinoma
>150-200 pg/ml
| p. 1928
140
Before testing for fasting gastrin levels to diagnose gastrinoma/ZES, PPIs should be discontinued at least how many days?
7 days
| p. 1928
141
What is considered to be pathognomonic of ZES?
Basal acid output (BAO) >15 meq/h
| p. 1928
142
The most sensitive and specific gastrin provocative test for the diagnosis of gastrinoma
Secretin study
| p. 1928
143
Treatment of choice for ZES
Proton pump inhibitors
| p. 1929
144
Favorable prognostic indicators for ZES
```
Primary duodenal wall tumors
Isolated lymph node tumor
Presence of MEN1
Undetectable tumor upon surgical exploration
(p. 1929)
```
145
Poor prognostic indicators for ZES
```
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
Most common presentation of Stress-related mucosal injury
GI bleeding
| p. 1929
147
Risk factors for bleeding in stress-related mucosal injury
Respiratory failure requiring mechanical ventilation
Coagulopathy
(p. 1929)
148
Stress ulcer after head trauma
Cushing's ulcer
| p. 1930
149
Stress ulcer after severe burns
Curling's ulcer
| p. 1930
150
Sucralfate use in endotracheal intubated patients has been associated with ___.
Aspiration pneumonia
| p. 1930
151
Treatment of choice for stress ulcer prophylaxis
Proton pump inhibitors
| p. 1930
152
Definition: histologically documented inflammation of the gastric mucosa
Gastritis
| p. 1930
153
Three phases of gastritis
Superficial gastritis
Strophic gastritis
Gastric atrophy
(p. 1930)
154
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
Superficial gastritis
| p. 1930
155
Phase of gastritis wherein inflammatory infiltrates extend deeper into the mucosa, with progressive distortion and destruction of the glands
Atrophic gastritis
| p. 1930
156
Phase of gastritis wherein glandular structures are lost and there is paucity of inflammatory infiltrates
Gastric atrophy
| p. 1930
157
Type of gastritis that spares the antrum
Type A gastritis
| p. 1931
158
Type of gastritis which is also known as autoimmune gastritis
Type A gastritis
| p. 1931
159
This type of gastritis has been associated with pernicious anemia
Type A gastritis
| p. 1931
160
Higher incidence of these specific histocompatibility haplotypes have been noted in Type A gastritis
HLA-B8
HLA-DR3
(p. 1931)
161
Type of gastritis which is antral-predominant
Type B gastritis
| p. 1931
162
More common form of gastritis (Type A / B?)
Type B gastritis
| p. 1931
163
Type of gastritis associated with H.pylori infection
Type B gastritis
| p. 1931
164
What type of disease/condition is associated with long term use of PPIs in older women?
Hip fracture
| p. 1921
165
Type of gastritis: mucosal lesion of unknown etiology that has a pseudotumoral endoscopic appearance
Russell body gastritis (RBG)
| p. 1932
166
Russell body gastritis is histologically defined by the presence of numerous plasma cells containing Russell bodies that express ____ and ____ light chains.
Kappa and lambda
| p. 1932
167
Very rare gastropathy characterized by large, tortuous mucosal folds
Menetrier's Disease
| p. 1932
168
Often etiology of Menetrier's Disease in children
CMV
| p. 1932
169
First line treatment for Menetrier's Disease
Cetuximab
| p. 1932
170
Three types of intestinal ischemia based on etiology
Arterioocclusive mesenteric ischemia
Non-occlusive mesenteric ischemia
Mesenteric venous thrombosis
(p. 1978)
171
Risk factors for arterioocclusive mesenteric ischemia
```
Atrial fibrillation
Recent myocardial infarction
Valvular heart disease
Recent cardiac or vascular catheterization
(p. 1979)
```
172
Type of intestinal ischemia which is the most prevalent gastrointestinal disease complicating cardiovascular surgery
Non-occlusive mesenteric ischemia
| p. 1979
173
Type of intestinal ischemia associated with the presence of a hypercoagulable state (protein C/S deficiency, anti-thrombin III deficiency, polycythemia vera, etc)
Mesenteric venous thrombosis
| p. 1979
174
What are Griffith's point and Sudeck's point?
Most common locations for colonic ischemia
| p. 1979
175
What are the two most common locations for colonic ischemia?
Griffith's point and Sudeck's point
| p. 1979
176
Splanchnic circulation can receive up to how many percent of the cardiac output?
30%
| p. 1979
177
In occlusive mesenteric ischemia, where do emboli preferentially lodge?
Superior mesenteric artery, distal to the origin of the middle colic artery
(p. 1979)
178
Intestinal ischemia that is disproportionate mesenteric vasoconstriction (vasospasm) in response to a severe physiologic stress (e.g. Shock)
Non-occlusive ischemia
| p. 1979
179
What disease/condition presents with severe, acute, nonremitting abdominal pain that is out of proportion to the physical findings?
Acute mesenteric ischemia
| p. 1979
180
Plain abdominal film findings for mesenteric ischemia
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
Air seen within the bowel wall in plain abdominal Xray of intestinal ischemia
```
Pneumatosis intestinalis
(p. 1979)
```
182
Screening test for mesenteric ischemia
Mesenteric duplex scan
| p. 1979
183
Highly sensitive test for intestinal ischemia
Dynamic CT angiography
| p. 1979
184
What is the gold standard for the diagnosis of acute arterial occlusive disease?
Angiography
| p. 1980
185
What is the management for acute arterial occlusive disease?
Laparotomy
| p. 1980
186
Markers for intestinal ischemia
```
D-dimer
Glutathione S-transferase
Platelet-activating factor (PAF)
Mucosal pH monitoring
(p. 1980)
```
187
On colonoscopy, MILD ischemic colitis is seen as?
Minimal mucosal erythema
| p. 1980
188
On colonoscopy, MODERATE ischemic colitis is seen as?
Pale mucosal ulcerations and evidence of extension to the muscular layer of the bowel wall
(p. 1980)
189
On colonoscopy, SEVERE ischemic colitis is seen as?
Severe ulcerations resulting in black or green discoloration of the mucosa, consistent with full-thickness bowel wall necrosis
(p. 1980)
190
Degree of reversibility of mild ischemic colitis
100% reversible
| p. 1980
191
Degree of reversibility of moderate ischemic colitis
50% reversible
| p. 1980
192
Degree of reversibility of severe ischemic colitis
Irreversible
| p. 1980
193
Diagnostic modality for mesenteric thrombosis
Abdominal Spiral CT with oral and IV contrast
| p. 1980
194
Among the types of intestinal ischemia/disorders, which has the best prognosis?
Mesenteric venous insufficiency
| p. 1981
195
What disease/condition presents as abdominal cramping and pain following ingestion of a meal, and often shows a malnourished patient with an abdominal bruit?
Chronic intestinal ischemia
| p. 1981
196
In equivocal cases after revascularization of intestinal ischemia, what can be administered to observe the pattern of bowel reperfusion?
1 gram of IV sodium fluorescein
| p. 1981
197
This occurs when the bowel twists on its mesenteric axis
Volvulus
| p. 1982
198
What area is most commonly affected in volvulus?
Sigmoid colon
| p. 1982
199
Risk factors for volvulus
```
Institutionalization
Presence of neuropsychiatric conditions requiring psychotropic medication
Chronic constipation
Aging
(p. 1982)
```
200
Also known as ileum and pseudo-obstruction
```
Functional obstruction
(p. 1982)
```
201
This is the condition in which dysmotility prevents intestinal contents from being propelled dismally but no mechanical blockage exists
```
Functional obstruction
(p. 1982)
```
202
Pseudo-obstruction of the colon
Ogilvie's syndrome
| p. 1982
203
What is Ogilvie's syndrome?
Pseudo-obstruction of the colon
| p. 1982
204
Epithelial necrosis can be identified within how many hours of intestinal obstruction?
Within 12 hours
| p. 1982
205
In intestinal obstruction, the most commonly cultured intraluminal organisms are?
E. coli
Streptococcus feacalis
Klebsiella
(p. 1982)
206
This results when the proximal and distal openings of a given bowel segment are both occluded
Closed-loop obstruction
| p. 1982
207
What is the most common precursor for bowel strangulation?
Closed-loop obstruction
| p. 1982
208
The risk for cecal perforation is greatest when the cecal diameter exceeds ____.
12 cm
| p. 1982
209
Cardinal signs of intestinal obstruction
```
Colicky abdominal pain
Abdominal distention
Eyes is
Obstipation
(p. 1983)
```
210
Patients with more proximal intestinal obstruction commonly present with less abdominal distention but more pronounced ___.
Vomiting
| p. 1983
211
Classical findings in plain abdominal Xray of small bowel obstruction
"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
"Coffee-bean" shaped dilated shadow in plain abdominal Xray may be seen in what condition?
Volvulus
| p. 1984
213
Most commonly used imaging modality for intestinal obstruction
CT scan
| p. 1984
214
CT scan findings of "bird's beak", a "c-loop", or "whorl"
Colonic volvulus
| p. 1984
215
This diagnostic modality is generally contraindicated in patients with firm evidence of complete or high grade bowel obstruction
Barium studies
| p. 1984
216
An acetylcholinesterase inhibitor which can stimulate colonic motility
Neostigmine
| p. 1985
217
Intravenous administration of this drug induces defamation and flats within 10 minutes in majority of patients with Ogilvie's disease
Neostigmine
| p. 1985
218
Treatment for cecal volvulus
Laparotomy or laparoscopic correction
| p. 1985
219
Treatment for sigmoid volvulus
Decompression using a flexible tube through a rigid proctoscope or sigmoidoscope
(p. 1985)
220
At operation, what is a defining feature of bowel obstruction?
Dilation proximal to the site of blockage with distal collapse
(p. 1985)
221
Where is the most common site of intestinal obstruction in patients with gallstone "ileus"?
Ileum (60%)
| p. 1985
222
In gallstone ileus, the gallstone enters the intestinal tract most often via what/where?
Cholecystoduodenal fistula
| p. 1985
223
Early postoperative mechanical bowel obstruction occurs within the first ___ weeks of operation.
6 weeks
| p. 1985
224
Most common emergency general surgical disease affecting the abdomen
Appendicitis
| p. 1985
225
Appendicitis is more common in men with a male-to-female ratio of ___.
1. 4:1
| p. 1985
226
Most important cause of excess morbidity and mortality in Appendicitis
Perforation
| p. 1985
227
Believed to be an important step in the development of appendicitis
Obstruction of the appendiceal lumen
| p. 1986
228
Patients with appendicitis who have had symptoms for more than ___ hours are more likely to perforate.
48
| p. 1986
229
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.
True
| p. 1986
230
True or false: In appendicitis, abdominal pain is experienced first before nausea.
True
| p. 1987
231
True or false: In appendicitis, nausea comes first before abdominal pain.
False
| p. 1987
232
True or false: In gastroenteritis, nausea comes first before abdominal pain.
True
| p. 1987
233
The absence of this symptom should question the diagnosis of appendicitis
Anorexia
| p. 1987
234
___ appendicitis are more likely to present with dysuria, urinary frequency, diarrhea, or tenesmus.
Pelvic
| p. 1987
235
Gynecologic diseases/conditions that may mimic appendicitis
Pelvic inflammatory disease
Ectopic pregnancy
Ovarian torsion
(p. 1987)
236
In appendicitis, maximal tenderness is classically identified where?
RLQ at or near the McBurney's point
| p. 1987
237
Where is McBurney's point?
1/3 of the way along a long originating at the anterior iliac spine running to the umbilicus
(p. 1987)
238
Gentle pressure in the LLQ of the abdomen may elicit pain in the RLQ
Rovsing's sign
| p. 1987
239
What is Rovsing's sign?
Gentle pressure in the LLQ of the abdomen may elicit pain in the RLQ if the appendix is located there
(p. 1987)
240
Most common presenting symptom of appendicitis?
```
Abdominal pain (>95%)
(p. 1987, Table 356-2)
```
241
What is obturator sign?
Internal rotation of the hip causes pain, suggesting the possibility of an inflamed appendix located in the pelvis
(p. 1987)
242
What does a positive obturator sign mean?
Suggests the possibility of an inflamed appendix located in the pelvis
(p. 1987, Table 356-4)
243
What is iliopsoas sign?
Extending the right hip causes pain alon posterolateral back and hip, suggesting retrocecal appendicitis
(p. 1987, Table 356-4)
244
What does a positive iliopsoas sign mean?
Suggests retrocecal appendicitis
| p. 1987, Table 356-4
245
Ultrasound findings suggesting the presence of appendicitis
Wall thickening
Increased appendiceal diameter
Presence of free fluid
(p. 1988)
246
Sensitivity and specificity of CT scan for diagnosing appendicitis
94 and 95%
| p. 1988
247
CT scan findings for appendicitis
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
What is the most common extrauterine general surgical emergency observed during pregnancy?
Appendicitis
| p. 1988
249
Why is diagnosing appendicitis difficult in pregnant women?
As the uterus enlarges, the appendix may be pushed higher along the right flank even to the RUQ
(p. 1988)
250
Fetal mortality rate in pregnant women with perforated appendicitis
20% or 4x greater
| p. 1988
251
What is the appropriate management in patients with appendicitis presenting with a mass (representing a phlegmon or abscess)?
```
Broad-spectrum antibiotics
Drainage if abscess >3 cm in diameter
Parenteral fluids
Bowel rest
(p. 1988)
```
252
In patients with appendicitis presenting with a mass (representing phlegmon or abscess), when can the appendix be safely removed?
6-12 weeks later (when the inflammation has diminished)
| p. 1988
253
What is the most common postoperative complications of appendicitis?
Fever
Leukocytosis
(p. 1988)
254
What are the cardinal signs and symptoms of peritonitis?
Acute severe abdominal pain with tenderness and fever
| p. 1989
255
Type of peritonitis which is commonly caused by the abnormal presence of physiologic fluids (e.g. Gastric juice, bile, pancreatic enzymes, blood, urine)
Aseptic peritonitis
| p. 1989
256
What forms the common bile duct?
Common hepatic duct and cystic duct
| p. 2075
257
Common bile duct enters the duodenum through the ___.
Ampulla of Vater
| p. 2075
258
The total daily basal secretion of hepatic bile is ___.
500-600 ml
| p. 2075
259
What are the three important mechanisms in regulating bile flow?
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
This is an aminophospholipid transferase "flippase" essential for maintaining the lipid asymmetry of the canalicular membrane
F1C1
| p. 2075
261
This is seen to be defective in progressive familial intrahepatic cholestasis type 1 (PFIC1) and benign recurrent intrahepatic cholestasis type 1 (BRIC1)
F1C1
| p. 2076
262
This pump is seen to be defective in progressive familial intrahepatic cholestasis type 2 (PFIC2) and benign recurrent intrahepatic cholestasis type 2 (BRIC2)
Bile salt export pump (BSEP)
| p. 2076
263
Mutations of ___ cause the Dubin-Johnson syndrome
An ionic conjugate export pump (MRP2)
| p. 2076
264
Defect in ___ results in progressive familial intrahepatic cholestasis type 3 (PFIC3)
Phospholipid export pump (MDR3)
| p. 2076
265
This pump is seen to be defective in sitosterolemia
Canalicular cholesterol and phytoestrogens transporter (ABCG5/G8)
(p. 2076)
266
This pump is seen to be defective in cystic fibrosis
Cystic fibrosis transmembrane regulator (CFTR)
| p. 2076
267
What are the primary bile acids?
Cholic acid
Chenodeoxycholic acid (CDCA)
(p. 2076)
268
The primary bile acids are conjugated with what amino acid/s before being secreted into the bile?
Glycine OR taurine
| p. 2076
269
What are the secondary bile acids?
Deoxycholate
Litocholate
Ursodeoxycholic acid (UDCA)
(p. 2076)
270
Micelles are molecular aggregates of ___.
Bile acids
| p. 2076
271
Unconjugated bile acids are absorbed along the entire gut by ___.
Passive diffusion
| p. 2076
272
The normal bile acid pool size is ___.
2-4 grams
| p. 2076
273
Normally, how many times does the bile acid pool circulate?
5-10 times
| p. 2076
274
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?
Fibroblast growth factor 19 (FGF19)
| p. 2076
275
Fibroblast growth factor 19 (FGF19) released by bile acids in the intestine functions to:
1) Suppress synthesis of bile acids from cholesterol by inhibiting CYP7A1
2) Promotes gallbladder relaxation
(p. 2076)
276
What receptor is a bile acid sensor that also represses bile acid synthesis?
Farnesoid X receptor (FXR)
| p. 2076
277
ABC65/G8 is upregulated by which receptor, which is also an oxysterol sensor?
Liver X receptor (LXR)
| p. 2076
278
Tonic contraction of the Sphincter of Oddi functions to:
1) Prevent reflux of duodenal contents into the pancreatic and bile ducts
2) Promote filling of the gallbladder
(p. 2076)
279
WHich hormone is released from the duodenal mucosa in response to the ingestion of fats and amino acids?
Cholecystokinin (CCK)
| p. 2076
280
What is/are the function/s of CCK?
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
The normal capacity of the gallbladder is ___ ml of bile.
30
| p. 2076
282
Clinically innocuous entity in which a partial or complete septum (or fold) separates the fundus from the body
Phrygian cap
| p. 2076
283
This condition predisposes to acute torsion, volvulus, or herniation of the gallbladder
Floating gallbladder
| p. 2076
284
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
Cholesterol stones
| p. 2076
285
Type of gallstone that is composed primarily of calcium bilirubinate
Pigment stones
| p. 2076
286
Type of gallstone that is classified into "black" and "brown" types
Pigment stones
| p. 2076
287
What is the rate limiting enzyme of hepatic cholesterol synthesis?
HMG-CoA reductase
| p. 2077
288
True or false: In patients without gallstones, dietary cholesterol increases biliary cholesterol secretion.
False, only occurs in patients with gallstones
| p. 2077
289
What gene mutation results in a deficiency of the enzyme cholesterol 7-hydroxylase (initial step in cholesterol catabolism and bile acid synthesis)?
CYP7A1 gene
| p. 2077
290
What gene mutation can cause defective phospholipid secretion into bile, thus resulting in cholesterol supersaturation of bile?
MDR3 gene
| p. 2077
291
Where do cholesterol monohydrate crystal nucleation and crystal growth probably occur?
Mucin gel layer
| p. 2077
292
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?
Binary sludge
| p. 2077
293
What typically forms a crescent-like layer in the most dependent portion of the gallbladder recognized by the characteristic echoes on UTZ?
Biliary sludge
| p. 2077
294
The presence of biliary sludge implies what two abnormalities?
1) The normal balance between gallbladder mucin secretion and elimination has become deranged
2) Nucleation of biliary salutes has occurred
(p. 2077)
295
True or false: Pregnancy is associated with biliary sludge formation.
True
| p. 2078
296
True or false: Rapid weight loss reduction through very-low calorie diet can cause biliary sludge.
True
| p. 2078
297
What are the two key changes during pregnancy that contribute to a "cholelithogenic state"?
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
Cholesterol gallstone disease occurs because of what 3 mechanisms?
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
Gallstones composed of either pure bilirubinate or polymer-like complexes with calcium and mucin glycoproteins
Black pigment stones
| p. 2078
300
Type of pigment stone that is more common in patients who have chronic hemolytic states, liver cirrhosis, Gilbert's syndrome, or cystic fibrosis
Black pigment stones
| p. 2078
301
Gallbladder stones in patients with ileal diseases, ileal resection, or ileal bypass are generally what type of pigment stones?
Black pigment stones
| p. 2078
302
What type of pigment stone is composed of calcium salts of unconjugated bilirubin with varying amounts of cholesterol and protein?
Brown pigment stones
| p. 2078
303
This type of pigment stone is caused by the presence of increased amounts of unconjugated, insoluble bilirubin in bile that precipitate to form stones
Brown pigment stones
| p. 2078
304
Deconjugation of an excess of soluble bilirubin mono- and diglucuronides may occur by spontaneous hydrolysis OR may be mediated by what enzyme?
Beta-glucuronidase
| p. 2078
305
What imaging test is very accurate in the identification of cholelithiasis (has replaced oral cholecystography)?
Ultrasound of the gallbladder
| p. 2078
306
In UTZ of the gallbladder, stones as small as ____ in diameter may be confidently identified
1. 5 mm
| p. 2078
307
In UTZ of the gallbladder, what does biliary sludge look like?
Material of low echogenic activity that typically forms a layer in the most dependent portion of the gallbladder
(p. 2078)
308
In UTZ of the gallbladder, how do you differentiate biliary sludge from gallstones?
Biliary sludge fails to produce acoustic shadowing
| p. 2078
309
True or false: Ultrasound of the gallbladder can be used to assess the emptying function of the gallbladder
True
| p. 2078
310
UTZ criteria to diagnose gallstones
Acoustic shadowing of opacities that are within the gallbladder lumen and that change with the patient's position (by gravity)
(p. 2078)
311
Plain abdominal film in cholelithiasis may be used in diagnosing what gallbladder/bile conditions?
```
Emphysematous cholecystitis
Porcelain gallbladder
Limey bile
Gallstone ileus
(p. 2078)
```
312
Imaging test that has historically been a useful procedure for the diagnosis of gallstones but is now regarded obsolete
Oral cholecystography
| p. 2078
313
Imaging/diagnostic test used for accurate identification of cystic duct obstruction with simultaneous assessment of bile ducts
```
Radioisotope scans (HIDA, DIDA, DISIDA, etc)
(Pp. 2078, 2079)
```
314
What is the most specific and characteristic symptom of gallstone disease?
Biliary colic
| p. 2079
315
True or false: Biliary colic is frequently nocturnal
True
| p. 2080
316
True or false: Up to 80% of persons with a symptomatic gallstones remain asymptomatic over up to 25 years
True
| p. 2080
317
The recommendation for cholecystectomy in a patient with gallstones should probably be based on assessment of what factors (three)?
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
Prophylactic cholecystectomy may be considered in what conditions?
1) Patients with very large gallstones (>3cm in diameter)
2) Patients with gallstones.in a congenitally anomalous gallbladder
(p. 2080)
319
What is the gold standard for treating symptomatic cholelithiasis?
Laparoscopic cholecystectomy
| p. 2080
320
In gallstone disease, UDCA may be used in radiolucent stones smaller than ____ in diameter.
5 mm
| p. 2080
321
Dose of UDCA
10-15 mg/kg/day
| p. 2080
322
True or false: Pigment stones are responsive to UDCA therapy
False
| p. 2080
323
True or false: Patients with cholesterol gallstone disease who develop recurrent choledocholithiasis after cholecystectomy should be on long-term treatment with UDCA
True
| p. 2080
