GASTRO Flashcards
(731 cards)
1
Q
Which causes caustic ingestion more often? Alkali or acid substance
A
Alkali
2
Q
Glucocorticoids si recommended in the treatment of corrosive esophagitis: true or false
A
false
3
Q
Most common location for pill to lodge?
A
mid-esophagus, nearing the crossing of the aorta or carina
4
Q
Typical symptom of Pill-induced esophagitis
A
sudden onset of chest pain and odynophagia developing over hours or awaken patient from sleep
5
Q
Manifestation of scleroderma esophagus
A
hypotensive LES adn absent esophageal peristalsis
6
Q
The pre-epithelial barrier of the mucosal defense of the stomach is composed of (2):
A
Mucous gel
Bicarbonate
7
Q
Bicarbonate is secreted into the mucous gel of the stomach by the epithelial cells to maintain a pH gradient of
A
pH 6-7
8
Q
Migration of the gastric epithelial cells to restore a damaged region following breach of the preepithelial barrier
A
restitution
9
Q
Play a central role in gastric epithelial defense/repair by regulating release of mucosal HCO3 and mucus, inhibit parietal cell secretion, and maintains mucosal blood flow and epithelial cell restitution
A
Prostaglandin
10
Q
2 prinicipal gastric secretory products capable of inducing mucosal injury
A
HCl
Pepsinogen
11
Q
Which occurs later in life? gastric ulcer or duodenal ulcer?
A
Gastric ulcer
12
Q
95% of duodenal ulcers are located in the:
A
1st portion of duodenum,
90% is located within 3 cm from the pylorus
13
Q
Type of gastric ulcer that is located in the gastric body, tend to be associated with low gastric acid production
A
Type I
14
Q
Type of gastric ulcer that occr in the antrum; gastric acid can vary from low to normal
A
Type II
15
Q
Type of gastric ulcer that occur within 3 cm from the pylorus, commonly accompanied by DUs, normal or inc gastric acid production
A
Type III
16
Q
Type of gastric ulcer that is found in the cardia, with low gastric acid production
A
Type IV
17
Q
Description of H. pylori
A
Gram negative, microaerophilic rod
18
Q
At what part of the stomach does the H. pylori typically resides?
A
Antrum
19
Q
Dormant form of H. pylori that facilitates survival in adverse conditions
A
Coccoid form
20
Q
Factors that are essential deteminants of H-pylori-mediated pathogenesis and colonization (3):
A
- outer membrane protein (Hop protein)
- urease
- vacuolating cytotoxin (Vac A)
21
Q
First step in infection by H. pylori is dependent on (2):
A
- bacteria’s mobility
2. ability to produce urease
22
Q
In the developing countries, how many percent of the population may be infected with H. pylori by age 20? How about in industrialized countries?
A
developing countries - 80%
industrialized countries - 20-50%
23
Q
2 factors that predispose to higher colonization rates of H. pylori.
A
- poor socioeconomic status
2. less education
24
Q
Risk factors for H. pylori infection (5):
A
- Birth or residence in a developin country
- Domestic crowding
- Unsanitary living conditions
- Unclean food or water
- exposure to gastric contents of an infected individual
25
Lipopolysaccharide of this organism has low immunologic activity compared to that of in other organisms
H. pylori
| may promote a smoldering chronic inflammation
26
Antral-predominant gastritis is seen in: DU vs GU
DUs
27
Corpus-dominant gastritis is seen in: GU vs DU
GU
| also in gastric atrophy and gastric carcinoma
28
How many percent of serious NSAID-related PUD complication is not preceeded with dyspepsia?
>80%
29
Pathophysiology of NSAID-inducecd ulcer?
Interruption of prostaglandin synthesis impairing mucosal defense and repai
30
Blood groip that has increased susceptibility to H. pylori infection?
Blood group O
| H. pylori preferentiaally binds to group O anyigen
31
Abdominal pain occurs 90 min to 3 hours after meal. DU vs GU
DU
32
Frequently relieved by food or antacids: DU vs GU
DU
33
Most discriminating symptom of DU
Pain that wakes up patient from sleep
| seen in 2/3 of DU, and 1/3 in NUD
34
Pain is precipitated by food. GU vs DU
GU
35
Nausea and weight loss is most common. GU vs DU
GU
36
When do you suspect that ulcer penetrated the pancreas?
dyspepsia becomes constant, NOT relieved by food or antacids, and radiates to the back
37
Ulcer complication characterized by sudden onset of severe generalized abdominal pain
Perforation
38
Ulcer complication characterized by worsening of pain with meals, nasuea, and vomiting of undigested food
Gastric outlet obstruction
39
Most frequent PE finding in PUD but with low predictive value
epigastric tenderness
40
PE finding of severely tender, board-like abdomen in PUD patients indicates
perforation
41
PE finding of succussion splash in PUD patients indicate
Gastric outlet obstruction
42
Most common complication of PUD
Bleeding
43
30-day mortality rate of GI bleeding
2.5-10%
44
80% of the mortality in PUD-related bleeding is due to nonbleeding causes, most commonly (3):
```
multiorgan failure (24%)
Pulonary complication (24%)
Malignancy (34%)
```
45
2nd most common complication of PUD
perforation
46
30-day mortality rate of PUD perforation
>20%
47
Form of perforation in which the ulcer bed tunnels into an adjacent organ
penetration
48
Duodenal ulcer penetrates most commonly in:
pancreas, causing pancreatitis
49
Gastric ulcer penetrates most commonly in:
left hepatic lobes
| may also cause gastrocolic fistulas
50
Least common PUD complication
gastric outlet obstruction
51
2 subcategories of functional dyspepsia:
Postprandial distress syndrome
| Epigastric pain syndrome
52
In what subset of patients with PUD will you test for H. pylori and give antibiotic therapy before any diagnostic evaluation?
in otherwise healthy patients and < 45 y.o
53
Most sensitive and specific examination of the upper GIT
Endoscopy
54
Biopsy urease test has a sensitivity and specificity of:
>90-95%
55
Mainstay of treatment of PUD (2):
Eradication of H. pylori
| Therapy/prevention of NSAID-induced disease
56
Give 3 examples of antacids:
AlMg
Calcium carbonate
Sodium bicarbonate
57
Antacid that has a side effect of milk-alkali syndrome
calcium carbonate
58
Give the 4 H2-receptor antagonists:
Cimetidine
Ranitidine
Famotidine
Nizatidine
59
Inhibit the basal and stimulated acid secretion
H2-receptor antagonists
60
Gynecomastia and impotence are adverse effects of this drug used for treatment of PUD:
Cimetidine
61
Mode of action of PPI
Irreversibly inhibit the H,K-ATPase thus inhibiting all phases of gastric acid secretion
62
Most potent acid inhibitory agents
PPI
63
Repeated daily dosing of PPI leads to _____, with basal and secretagogue-stimulated acid production being inhibted by ______ after _______ of therapy
progressive acid inhibition
>95%
1 week of therapy
64
Anemia that is a side effecr of PPI
Vitamin B12-deficiency anemia (due to inhibition of IF production (uncommon)
65
Adverse effect of PPI that will interfere the absorption of certain drugs
Hypochlorydia
66
PPI that inhibit hepatic CYP450 (2):
Omeprazole
Lanzoprazole
Not with newer PPIs
67
Drug that is converted to a viscous paste within stomach and duodenum and bound to active ulcers
Sucralfate
68
Most common side effect of sucralfate
constipation
69
adverse effects of short-term use of bismuth=-containing preperations (3):
black stools
constipation
darkening of tongue
70
Adverse effect of long-term use of bismuth-containing preparations
neurotoxicity
71
Prostaglandin analogue that is used as cytoprotective agents as treatment of PUD
Misoprostol
72
Most common adverse effect of prostaglandin analogue
diarrhea
73
Greatest influence of H. pylori therapy in the management of PUD
prevent recurrence of PUD
74
According to teh American College of Gastoenterology clinical guidelines, the indications for testing and treating H. pyllori are (4):
1. Inidviduals aged < 60 with uninvestigated dyspepsia
2. with prior history of PUD ad will be given an NSAID
3. Undergone resection of early gastric cancer
4. Unexplained IDA and ITP
75
In H. pylori treatment, aim an initial eradication rate of :
85-90%
76
First effective triple regimen fo H. pylori
Bismuth + metronidazole + tetracycline
77
Salvage therapies for treatment of patients with failure of H. pylori eradication with triple thearpy (4)
1. Quadruple therapy (PPI, Bismuth, tetracycline, metronidazole or clarithromycin) for 14 days
2. PPI + amoxicillin + rifabutin for 10 days
3. Levofloxacin + amoxicillin + PPI for 10 days
4. Furazolidone + amoxicillin + PPI for 14 days
78
Usually used triple therapy for H. pylori eradication:
PPI BID
Clarithromyci 500 mg BID
Amoxicillin 1g BID or Metronidazole 500 mg TID
for 14 days
79
If there is still failure of eradication of H. pylori even with salvage therapy, what is your next step?
Do culture and sensitivity
80
For patients with dyspepsia, if teh non-invasive H. pylori testing revealed negative, how will you treat the patient?
empiric treatment with H2 blocker or refer to gastroenterologist
81
How will you confirm eradication of H. pylori?
Urea breath test
82
If gastric ulcer biopsy is negative, what diagnostic procedure will you do next? Include rationale
repeat endoscopy at 8-12 weeks after to document healing. if still with ulcer, do repeat biopsy
70% of GUs are eventually found malignant
83
Refractory ulcer is GU that fails to heal after _____ and a DU that does not heal after _____ of therapy
12 weeks
| 8 weeks
84
Tests you should do to exclude ZES (2):
fasting gastrin
| secretin stimulation test
85
90% of refractory ulcer heal after this treatment (include duration)
high dose PPI for 8 weeks
86
Necessary component for surgical operations for duodenal ulcer
vagotomy
87
Truncal or selective vagotomy preserve these branches
celiac and hepatic branches
88
Type of vagotomy that has higher ulcer recurrence but with lowest overall complication rates
Highly selective vagotomy
89
Type of procedure that has lowest rates of ulcer recurrence but has the highest complication rate
vagotomy + antrectomy
90
Gastroduidenostomy is a reanoastomoses post-antrecctomy that is also known as
Billroth I
91
Gastrojejunostomy is a reanoastomoses post-antrecctomy that is also known as
Billroth II
92
Surgical procedure for antral ulcer
antrectomy (including the ulcer) with a Billroth I anastomosis
93
Surgical procedure for ulcer located at the esophagogastric junction
subtotal gastrectomy with Roux-en-Y esophagogastrojejunostomy (Csende's procedure
94
Ulcers developing at the site of anastomosis after partial gastric resection
stomal or marginal ulcer
95
Most frequent presenting complaint of recurent ulcer
epigastric abdominal pain, with severity and duration more progressive than observed with pre-surgical DUs
96
Medical therapy for postoperative ulceration
H2-receptor antagonists (effective in 70-90% of patients)
97
Afferrent Loop Syndrome is associated with what type of anastomosis?
Billroth II
98
2 types of afferent loop syndrome
1. bacterial overgrowth in the afferent limb secondary to stasis (most common)
2. severe abdopminal pain and loating
99
What type of post-op complication causes post=prandial abdominal pain, bloating, diarrhea with malabsorption of fats and vitamin B12
afferent loop syndrome
100
What post op complication causes severe abdominal pain and bloating 20-60 min after meals, often followed by nausea and vomiting of bile-containing material, with improvemnt of symptoms after emesis?
afferent loop syndrome
101
Causes series of vasomotor and GI signs and symptoms and occurs in patients who have undergone vagotomy and drainage?
Dumping syndrome
102
Early dumping opccurs how many minutes after meals?
15-30 mins
103
Late dumping syndrome occurs how many minutes after meals?
90 min to 3h
104
Post-op complication manifested as crampy abdominal discomfort, nausea, diarrhea, belching, tachycardia, palpitations, diaphoresis, light headedness, and rarely syncope?
Early dumping syndrome
105
Post-op compl;ication that is causd by rapid emptying of hyperosmolar gastric contents into the smalal intestine causing fluid shift into the gut lumen with plasma volume contraction and acute intestinal; distention and release of vasoactive GI hormones
Early dumping syndrome
106
Post-op complication that is predominated by vasomotor symoptoms such as ;light-headedness, diaphoresis, palpitations, tachycardia, syncope.
Late dumping syndrome
107
What is the mechanism of the late dumping syndrome?
hypoglycemia from excessive insulin release
108
What precipitates dumping syndrome? (3)
1. meals ricjh in simple carbohydrates
2. high osmolarity
3. large fluids
109
Cornerstone therapy for dumping syndrome
dietary modification
110
Alpha-glucosidase inhibitor that may be beneficial in late phase of dumping
Acarbose
111
Dietary modification for dumping syndrome
small, multiple (6) meals free of simple carbohydrates + NO liquid during meals
112
Post-vagotomy diarrhea most commonly follows what type of procedure?
truncal vagotomy
113
Post-op complication causing intermittent diarrhea occuring 1-2 h after meals
Post-vagotomy diarrhea
114
Treatment of post-vagotomy dirrhea (3)
Diphenoxylate or loperamide for symptom control
cholestyramine for severe cases
surgical reversal of a 10-cm segment of jejunum
115
Complication post-partial astrectomy with abdominal pain, early satiety, nausea, vomiting with only mucosal erythema of the gastric remnant
Bile reflux gasrtopathy
116
treatment of bile reflux gastropatrhy (3)
prokinetic agents
cholestyramine
sucralfate
117
This type of cancer increases in incidence in gastric stump 15 years after rsection, 4-5x increase risk 20-25 years post-resecryion
Gastric adenocarcinoma
118
Gastric acid hypersecretion due to unregulated gastrin release from a non-beta cell well-differentiated neuroendocrine tumor that is curable by surgical resection in ~40% of patients
Zollinger-Ellison Syndrome
119
ZES is associated with what type of neuroendocrine tumor?
Multiple endocrine neoplasia (MEN) type I
120
Hypergastrinemia with gastrin-stimulated acid hypersecretion and histamine release
Zollinger-Ellison Syndrome
121
Gastrinoma triangel is composed of:
1. confluence of systic and common bile duct
2. junction of 2nd and 3rd portions of the duodenum
3. junction of the neck and body of the pancreas
122
Most common non-pancreatic lesion in ZES
duodenal tumors (50-75% of gastrinomas)
123
Most common clinical manifestation of ZES
PUD
124
2nd most common clinical manifestation of ZES
Diarrhea
125
3 involved organs in MEN I syndrome
1. parathyroid
2. pancreas
3. pituitary
126
First diagnostic step for evaluation of ZES
obtain a fasting gastrin level
127
Prior to serum gastrin levels, when should you stop PPI, H2-receptor antagonist and antacids prior to testing?
PPI - 7 days prior
H2-receptor antagonist - 24 hrs prior
Antacids - 12 hours prior
128
During endoscopy pH measurement, what pH suggests gastrinoma?
pH < 3
| for pH > 3, need a formal gastric acid analysis
129
In the presence of hypergastrinemia, what level of BAO is considered pathognomonic for ZES?
> 15 mEq/h
130
BAO/MAO ratio that is highly suggestive of ZES
>0.6
131
Test that is used to differentuate between the causes of hypergastribnemia and useful in patients with indeterminate acid secretory studies
Gastrin provocative tests
132
Most sensitive and specific provocative tests for diagnosis of gastrinoma
Secretin stimulation test
133
Secretin stimulation test result that is suggestive of ZES
Gastrin of >/= 120 pg within 15 min of secretin injection
134
When should you stop PPI prior to a secretin stimulation test?
1 week before
135
2 gstrin provicative tests
1. secretin stimulation test
| 2. calcium infusion study
136
Functional imaging study of choice for ZES tumor localization
PET-CT with Ga-DOTATATE (if available)
137
Goals for treatment of ZES (3):
1. ameliorate signs and symptoms related to hormone overproduction
2. curative resection of the neoplasm
3. control tumor growth in metastatic disease
138
Treatment of choice for ZES
High dose PPI
| Omeprazole or lanzoprazole 60 mg in divided doses in 24-h
139
Treatment of ZES that inhibits effects of gastrin release from receptor-bearing tumors and inhibits gastric acidsecretion to some extent
Octreotide
140
Adjunct to PPI in the treatment of ZES
Octreotide
141
Definitive cure for ZES
Surgery
142
When do yopu treat patients wioth metastatic gastrinoma?
therapy may be delayed until with evidence of tumor progression or refractory symptoms with PPI
143
Favorable prognostic indicators for ZES (4):
1. Primary duodenal wall tumors
2. Isolated lymph node tumor
3. Undetectable tumor upon surgical exploration
4. Presence of MEN 1
144
Poor outcome indicators for ZES (6):
1. shorter disease duration
2. higher gastrin levels (>10,000 pg/mL)
3. large pancreatic primary tumor (>3 cm)
4. metastatic fisease (to lymph node, liver, bone)
5. Cushing's syndrome
6. rapid growth of hepatic metastases
145
Acute erosive gastric mucosal changes or frank ulceration with bleeding in patients suffering from shock, sepsis, massive burns, severe trauma, head injury
Stress-imduced gastritis or ulcers
146
Usual location of stress-induced gastritis or ulcers
fundus and body - acid-producing portions of the stomach
147
UGIB occur at what hour after acute injury or insult in stress-induced gastritis or ulcer?
48-72 hours
148
Ulcer that occur after head trauma
Cushing's ulcer
149
Ulcer that occur after severe burns
Curling's ulcer
150
Mortality rate of UGIB due to stress ulcer if with clinically important GI bleeding
> 40%
151
Preventive measure for stress ulcer is only given for patients who are high-risk such as with (4)
1. mechanical ventilation
2. coagulopathy
3. multiorgan failure
4. severe burns
152
Prophylaxis of choice for stress ulcer
PPIs
153
Most common cause of acute gastritis
infection
154
Rare, potentially life-threatening disorder caused by bacterial infection of the stomach
phlegmonous gastritis
155
High risk groups for phlegmonous gastritis (3)
1. elderly
2. alcoholics
3. AIDS
156
Type of chronic gastritis with inflammatory changes limited to lamina propria of the surface mucosa
Superficial gastritis
157
Type of chronic gastritis where inflammatory infiltrate extends deeper into the mucosa, progressive distortion and destruction of the glands
Atrophic gastritis
158
Final stage of chronic gastritis with loss of glandular structures, paucity of inflammation, thinned-out mcuosa
Gastric atrophy
159
Morphologic transformation of gastric glands in gastric atrophy
intestinal metaplasia
160
type of chronic gastritis that is an important predisposing factor for gastric cancer
gastric atrophy
161
type of chronic gastritis that is predominantly involve the fundus and body with antral sparing
Type A gastritis
162
Autoimmune gastritis is what type
Type A gastritsi
163
Type of gastritis that is traditionally associated with pernicious anemia in the presence of circulating antibodies against parietal cells and IF
Type A gastritis or autoimmune gastritis
164
2 types of antibodies presnt in autoimmune gastritis and what is more specific?
anti-IF antibodies - more specific
| Parietal cell antibodies
165
Associated diseases in type A gastritis (2):
Addison's
| Vitiligo
166
More common form of chronic gastritis (based on involvement)
Type B gastritis
167
Type of chronic gastritis that commonly involve the antrum
tyep B gastritis
168
Type of chronic gastritis that is caused by H. pylori infection
Type B gastritis
169
Type of chronic gastritis that convert to pan-gastritis
Type B gastritis
170
H. pylori infection can lead to cancer. Give 2 example
gastric cancer
| MALT lymphoma
171
If chronic gastritis has signs of intestinal metaplasia, how often will you do surveillance endosccopy?
every 3 years
172
Treatment for eosinophilic gastritis
glucocorticoids
173
Gastritis that is associated with several systemic disease and Crohn's diseae
Granulomatous gastritis
174
Rare disease characterized by large tortous gastric mucosal folds with male predominance
Menetrier's disease
175
Menetrier's disease commonly involves mucosal folds of:
body and fundus, with antral sparing
176
Pathology of this disease is massive foveolar hyperplasia replcing most of the chief and parietal cells, and is not considered as gastritis
Menetrier's disease
177
Etiology of Menetrier's disease
unknown in adults, CMV in children
178
First-line therapy for Menetrier's disease
Cetuximab or anti-EGFR
179
Surgical procedure for menetrier's disease
total gastrectomy
180
Age of onset oof UC and CD
2nd to 4th decade and 7th to 9th decade
181
UC vs CD: smoking prevents disease
UC
| Causes disease in CD
182
UC vs CD: Oral contraceptive increase risk of disease
Crohn's disease
183
UC vs CD: Appendectomy is protective
UC
184
UC vs CD: Vitamin D supplementation hasprotective effect
CD
185
If a apatient has IBD the lifetime risk that a first-degree relative will be affected is ___
~10%
186
Most common CD phenotype in East Asia
Ileocolonic CD
187
X-linked recessive disorder that is associated with colitis, immunodeficiency, severely dysfunctional platelets, and thrombocytopenia
Wiskott-Aldrich syndrome
188
Severe, refractory IBD that is caused by deficient IL-10 and IL-10 receptor function
Early-onset IBD
189
A state of commensal microbiota inpatients with both UC and CD
Dysbiosis - presence of microorganism that drive disease to which the immune response is directed and/or loss of microorganisms that hinder inflammation
190
UC vs CD: Usually involves the rectum
UC
191
In UC, ____ of patients have disease limited to the rectum and rectosigmoid, ____have disease extending beyond thesigmoid but not involving the whole colon, and ____ have total colitis
40-50%
30-40%
20%
192
UCvs CD: mucosa is erythematous and has a fine annualr surface that resembles sandpaper
mild UC
| in severe diseae, hemorrhagic, edematous, adn ulcerated
193
UC vs CD: complications are tpoxic colitis or megacolon, and perforation
UC
194
UC vs CD: The process is limited to the mucosa and superficial submucosa, with deeper layers unaffected except in fulminant disease
UC
195
UC vs CD: the neutrophils invade the epithelium, usually in the crypts, giving rise to cryptitis and, ultimately, to crypt abscesses
UC
196
In CD, ____ of patients have small bowel disease alone, ____ have disease involving both the small and large intestines, and ___ have colitis alone
30-40%
40-55%
15-25%
197
IN the 75% of patients with small intestinal CD, 90& involve the
terminal ileum
198
UC vs CD: rectum is usually spared
CD
199
UC vs CD: segmental with skip areas
CD
200
UC vs CD: rarely involve the liver and pancreas
CD
201
UC vs CD: transmural process
CD
202
UC vs CD: endoscopically, apthous or small superficial ulcerations characterize mild disease
CD
203
UC vs CD: in more active disease, stellate ulcerations fuse longitudinally and transversely to demarcate islands of mucosa that frequently are hstologically normal resulting to cobblestone appearance
CD
204
UC vs CD: focal inflammation and formation of fistula tracts occur
CD
205
UC vs CD; Granulomas are characteristic feature
CD
206
Major symptoms of UC (5):
```
diarrhea
rectal bleeding
tenesmus
passage of mucus
crampy abdominal pain
```
207
Diarrhea in UC is often
nocturnal and postprandial
208
Specific marker for dtecting iintestinal inflammation
fecal lactoferrin
209
Marker that dtects relpse of IBD and detect pouchitis
Fecal calprotectin
210
Differentiate mild, moderate adn severe UC in terms of: Bowel movement
Mild: < 4/day
Moderate: 4-6/day
Severe: > 6 per day
211
Differentiate mild, moderate adn severe UC in terms of: blood in stool
Mild: small
Moderate: moderate
Svere: severe
212
Differentiate mild, moderate adn severe UC in terms of: fever
mild: none
moderate: <37.5
severe: >37.5
213
Differentiate mild, moderate adn severe UC in terms of: tachycardia
mild: none
moderate: <90
severe: >90
214
Differentiate mild, moderate adn severe UC in terms of: anemia
mild: mild
Moderate: > 75% of normal Hgb
Severe: <75% of normal Hgb
215
Differentiate mild, moderate adn severe UC in terms of: ESR
Mild: <30 mm
Severe: > 30mm
216
Differentiate mild, moderate adn severe UC in terms of: endoscopic appeaance
Mild: erythema, decreased vascular pattern fine granularity
Moderate: marked erythema, coarse granularity, absent vascular markings, contact bleeding, no ulcerations
Severe: spontaneous bleeding, ulcerations
217
In massive hemorrhage due to UC, when is colectomy indicated?
when a patient required 6-8 u of blood within 24-48 hrs
218
Defined as a transverese or right colon with a diameter of > 6 cm
Toxic megacolon
219
Toxic megaccolon involves what segment of colon in UC? diameter?
transverse and righ colon
| > 6 cm
220
Most dangerous complication of UC
Perforation
221
In the presence of intestinal stricture, when is surgery indicated?
when the stricture prevents passage of the colonoscope
222
2 patterns of CD
fibrostenotic obstructing pattern
| penetrating fistulous pattern
223
this factor influences the clinical manifestion of D
site of disease
224
Most common site of inflammation in the ileocolitis CD
terminal ileum
225
usual presentation of ileocolic CD
chronic history of recurrent episodes of right lower quadrant pain and diarrhea, pain is usually colicky and preceds and relived by defecation
226
Seen as "string sign" on barium studies due to severely narrowed loop of bowel, which makes the lumen resemble a frayed cotton string
ileocolic CD
227
Characteristic features of jejunoileitis CD
malabsorption and steatorrhea, with nutritional deficiencies
| diarrhea
228
Clinical manifestations of CD colitis (5):
```
low-grade fever
malaise
diarrhea
crampy abdominal pain
hematochezia (sometimes)
```
229
Signs and symptoms of gastroduodenal disease in CD
nauea
vomiting
]epigastric pain
H. pylori - negative
230
Most commonly involved site in gastroduodenal CD
2nd portion of the duodenum
231
markers that are used to distinguish IBD from IBS (2)
fecall lactoferrin and calprotectin levels
232
The earliest macroscopic findings of colonic CD
apthous ulcers
233
Perforation in CD usually involves what site?
ileum
234
UC vs CD: intraabdominal and pelvic abscess occur in 10-30% of patients
CD
235
UC vs CD: increased titers of anti-saccharomyces cerevisiae antibodies
CD
236
UC vs CD: increased p-ANCAs levels
UC
237
Term for IBD wherein UC and CD are initiialy impossible to differentiate
indeterminate colitis
238
Infectious disease that mimic the endoscopic appearance of severe UC and can cause a relapse of established UC
campylobacter colitis
239
UC vs CD: blood and mucus in stool is more common
UC
240
UC vs CD: systemic symptosms are more common
CD
241
UC vs CD: pain is more common
CD
242
UC vs CD: abdominal mass is more common
CD
243
UC vs CD: significant perineal disease
CD
244
UC vs CD: small intestinal and colonic obstruction are more common
CD
245
UC vs CD: responds to antibiotics
CD
246
UCvs CD: recurrence after surgery is common
CD
247
UC vs CD: continuous disease
UC
248
UC vs CD: stricture is more frequent
CD
249
Similar to CDbut the mucosal abnormalities are limited to the sigmoid and descending colon
Diverticular-associated colitis
250
A differential diagnosis of IBDcharacterized by sudden onset of left lower quadrat pain, urdency to defecate, and the passage of bright red blod per rectum
ischemic colitis
251
Differential diagnosis of IBD that is caused by impaired evacuation and failure of relaxation of the puborectalis muscle
Solitary rectal ulcer syndrome
252
2 common drugs used in a hospital setting that mimic IBD
ipilimumab
mycophenolate mofetil
etanercept (case reports only)
253
2 atypical colitides
Collagenous colitis
lymphocytic colitis
completely normal endoscopic appearance
254
Inflammatory process that arises in segments of the large intestine that are excluded from the fecal stream, and usually occurs in patients with ileostomy or colostomy
diversion colitis
255
Difference of diversioon colitis from UC
crypt architecture is normal
256
Percentage of IBD patients that have at least one extraintetsinal disease manifestation
1/3
257
Extraintestinal manifestation of IBD that is characterized by hot, red, tender nodules measuring 1-5 cm in diameter and are found on the anterior surface of the lower legs, ankles, calves, thighs, and arms
eyrthema nodosum
258
Extraintestinal manifestation of IBD characterized by lesions that begin as pustules and spreads concentrically to rapidly undermine healty skin in the on the dorsal surface of the feet and legs, but may occur on the arms, chest, stoma, and even face.
Pyoderma gangrenosum
259
UC vs CD: -perianal skin tags in 75-80% of patients
CD
260
UC vs CD: pral mucosal lesions are more common
CD
261
UC vs CD: peripheral arthritsi is more common
CD
262
Characteristics of peripheral arthritis in IBD
asymmetric, polyarticular, and migratory, most often affecting the large joints, and worsens with exacerbations of bowel activity
263
UC vs CD: Aknylosing spondylitis is more common
CD
264
IBD with ankylosing spondylitis is associated with this antigen
HLA-B27 antigen
265
UC vs CD: uveitis is more common
equal
266
UC vs CD: episcleritis is more common
CD
267
An extraintestinal manifestation of IBD that is characterized by both intrahepatic and extrahepatic bile duct inflammation and fibrosism frequently leading to biliary cirrhosis and hepatic failure
primary sclerosing cholangitis
268
UC vs C: primary sclerosing cholangitis is more common
UC
269
Antibodies present in both IBD and PSC
pANCA
270
Gold standard diagnostic for PSC
ERCP - gold standard
| MRCP - sensitive, specific and safer
271
Priamry scclerosing cholangitis increase risk of what cancer? IBD and PSC will increase risk of what cancer?
cholangiocarcinoma
| colon cancer
272
Variant of PSC with normal cholangiography, and sometimes referred to as pericolangitis, and with better prognosis than classic PSC
small-duct PSC
273
Nephrolithiasis seen in CD is composed of what stone?
calcium oxalate
274
UC vs CD: nephrolithisis is more common
CD
275
UC vs CD: nephrolithisis is more common
CD
276
Medcal therapy for IBD (8)
```
5-ASA
Glucocorticoid
Antibiotics (for CD)
Azathioprine and 6-MP
Methotexate
Cyclosporine
Tacrolimus
Biologic therapies
```
277
Active ingredient of sulfasalazine
5-ASA and mesalamine
278
Supplements that should be given along with sulfasalazine
folic acid
279
A once-a-day formulation of mesalamine that is designed to release mesalamine in the colon
Lialda
280
A once-a-day formulation containing encapsulated mesalamine granules that delivers mesalamine to the terminal ileum and colon via proprietary extended release mechanism
Apriso
281
Mesalamine formulation that uses an ethylcellulose coating to allow water absorption into small beads containing the mesalamine
pentasa
282
Most common side effects of 5-ASA (4)
headaches
nauseas
hair loss
abdominal pain
283
Dose of glucocorticoid for moderate to severe UC that is unresposve to 5-ASA
Prednisone 40-60mg/day
hydrocortisone 300mg/d
methylprednisolone 40-60 mg/d
284
A new glucocorticoid for IBDthat is released entirely in the colon and has minimal to no glucocorticoid side effects. include dose
Budesonide 9 mg/d for 8 weeks with no tapering for UC
| ileal-release budesonide 9mg/d for 2-3 months and then tapered
285
Pouchitis in UC, which occurs in about 30-50% of UC patients after colectoy and IPAA usually responds to these 2 antibiotics (with dosage)
metronidazole 15-20 mg/kg per day in 3 divided doses
| ciprofloxacin 500mg BID
286
active end product of azathioprine and 6-MP
thioinosinicc acid
287
adverse effect of azathioprine and 6-MP that occurs on 3-4% of patient, typically presenting within the 1st few weeks of therapy, and is completely reversible when the drug is stopped
pancreatitis
288
Methotrexate inhibits what enzyme
dihydrofolate reductase
it also decrease production of IL-1
289
lipophilic peptide with inhibitory effects on both the cellular and humoral immunity, blocks production of IL-2, and inhibits calcineurin
cyclosporine
290
Common side effects of cyclosporine (7):
```
hypertension
gingival hyperplasia
hypertrichosis
paresthesias
tremors
headaches
electrolyte abnormalities
```
291
A macrolide antibiotic with immunomodulatory properties similar to cyclosporine, nut is 100 times more potent than CSA and not dependent on bile or mucosal integrity for absorption
Tacrolimus
292
the first biologic therapy approved for oderate to severely active IBD
infliximab
293
chimeric IgG1 antibody against TNF-a
infliximab
294
Recombinant human monoclonal IgG1 antibody containing only human peptide sequences and is injected subcutaneously
Adalimumab
295
A pegylated form an anti-TNF Fab portion of an antibody administered SC once a month
Certolizumab
296
ACCENT I and ACCENT II
A crohn's disessae clinical trial evaluating infliximab in a new long-term treatment regimen
40% of patients who experience initial response will maintain remission for at least 1 year with repeated infusions of infliximab every 8 weeks
297
SONIC trial
study of biologic and immunomodulator-naive patients with crohn's disease
infliximab plus azathioprine > infliximab > azathoprine
298
CHARM trial
Crohn's trial of the Fully Human Adalimumab for Remssion Maintenance
299
PRECISE II trial
pegylated antibody fragment evaluation in Crohn's disease
300
A recobinant humanized IgG4 antibody against a4-integrin that has been shown to be effective in induction and maintenance of patients with CD
natalizumab
301
adverse efect of natalizumab which is the reason why it is no longer widely used
progressive multifocal leukoencephalopathy (PML)
302
most important risk factor for development of PML in natalizumab user
exposure to JC polyomavirus
other risk factors:
longer duration of treatment
prior treatment with an immunosuppressant medication
303
a monoclonal antibody directed against a4b7 integrin that has the ability to convey gut-selective immunosuppression
vedolizumab
304
biological product that is highly similar to the reference product not withstanding minor differences in clinically inactive components
biosimilars
305
nutritional therapies for IBD
bowel rest and TPN
306
operation of choice for UC
ileal pouch/anal anastomosis (IPAA)
307
major complication of surgical therapy for UC
bowel obstruction
308
most frequent complication of IPAA
pouchitis
309
the need for surgery in CD is related to (2)
duration of the disease
| site of involvement
310
most frequently performed operation for CD
surgical resection of the disease segment
311
when will you do the colonoscopy after surgical procedrue for CD
after 6 months
312
T or F: fertility rates of patients with quiescent IBD is normal
True
313
part of the female reproductive system that can be scarreed by the inflammatory process of CD
right fallopian tube (due to proximity to the terminal ileum)
314
preferred route of delivery for patients with IBD
cesarean delivery
315
female patients with IBDmust be in remisiion ____ before conception
6 monhs
316
safest antibiotics that can be used for CD in pregnancy
Ampicillin adn cephalosporins
metronidazole - may be used in the 2nd and 3rd trimester
ciprofloxacin - contraindicated
317
extensive colitris is defined as involvement of
> 1/3 of the colon
318
risk factors for cancer in UC (7)
```
long duration diseae
extensive disease
family history of colon cancer
PSC
colon stricture
post-inflammatory pseudopolyp (UC)
bypassed colon segments (CD
```
319
Patients with CDhave increased risk of these malignancies (4)
NHL
leukemia
myelodysplastic syndrome
cancer in the lower rectum and anal canal (squamous cell carcinoma) - for those with severe perianal disease
320
Saclihe herniation of the entire bowel wall
True diverticulum
321
Protrusion of the mucosa through the muscularis propria of the colon
False or pseudodiverticulum
322
most common type of diverticulum affecting the colon
False or pseudodiverticulum
323
Where is the sitre of protrusion in False or pseudodiverticulum?
site of penetration of nutrient artery or vasa recti through muscularis propria
324
Common location of diverticular disease globally? among asians?
left and sigmoid colon and rectal sparing
in asian, 70% in the right colon and cecum
325
inflammation due to retention of particulate material within diverticular sac and formation of a fecalith
diverticulitis
326
complication of diverticular disease (2)
perforation
| bleeding
327
most common cause of hematochezua i patients > 60 years
colonic diverticular henorrhage
328
Percentage of patients with diverticulosis who will have GI bleeding
20%
329
risk factors for bleeding in diverticular disease (3(
hypertension
atheroscleosis
Aspirin and NSAIDs use
330
best diagnostic test for localization of massive bleeding of diverticular disease in otherwise stable patients
angiography
may also used as therapeutic by occluding the bleeding using coil
331
for bleeding diverticular disease patients who are on anticoagulant, what is the treatment in order to eliminate risk of further bleeding
```
segmental resection
subtotal colectomy (if bleeding sites are not localized)
```
332
inidcation for emergent surgery for bleeding diverticular disease
unstable patients
| 6 unit bleed within 24-hr
333
clinical manifestation of acute uncomplicated diverticulitis or SUDD (symptomatic uncomplicated diverticular disease) (4)
fever
anorexia
LLQ pain
obstipation
334
clinical manifestation of diverticular perforation
generalized peritonitis
335
clinical presnentation of pericolonic abscess of diverticular disease (2)
localized peritonitis
| abdominal distension
336
Complication of diverticular disease (4)
abscess - 16%
perforation - 10%
stricture - 5%
fistula - 2%
337
best diagnostic test for diverticulitis
CT scan
338
CT scan criteria for diverticulitis (4)
sigmoid diverticula
thickened colonic wall > 4 mm
inflammation within the pericolic fat
+/- collection of contrast media or fluid
339
When will you do colonoscopy after an attack of diverticular diseae?
after 6 weeks to rule out sigmoid malignancy
340
perforated diverticular disease staging
HInchey classification system
341
Purpose of the Hinchey claddification system
predict outcome following surgical management of complicated diverticular disaease
342
best management for asymptomatic diverticular disease
lifestyle modifications
fiber-rich diet
avoid smoking
343
initial management of symptomatic uncomplicated diverticular disease
bowel rest
| antibiotics
344
inications for hospitalization of divertocular disease patients (4)
unable to take oral therapy
several comorbids
fails to improve in the ourpatient therapy
complicated diverticultis
345
Recommended antibiotics for acute diverticulitis
3rd gen cephalosporin or ciprofloxacin + metronidazole
add ampicillin for non-responders for enterococci coverage
346
mainstay management for ppost acute diverticulitis episode
symptom prevention
347
risk factors for recurrence of diverticulitis (3)
younger age
diverticular abscess
frequent attacks (>2 per year)
348
poorly absorbed broad-spectrum antibiotic associated with 30% less frequent recurrent symptoms of diverticulitis
rifaximin
349
Hinchey stage Ia
pericolic phlegmon
350
Hinchey stage Ib
pericolic abscess
351
Indications for CT-guided percutaneous drainage of Hinchey Ib adn II diverticular disease
> 3 cm + well-defined wall
abscess < 5 cm - resolve with antibiotic therapy
352
Contraindications for CT-guided percutaneous draignage of diverticular abscess (3)
no percutaneous access route
pneumoperitoneum
fecal peritonitis
353
most common cause of fecal incontinence
obstetric injury of the pelvic floor
354
fecal incontinence in aduts is most common in this population
women >65 y, especially parous
355
in the management of fecal incontinence, this helps strengthen external sphincter muscle while training patient to relax with defecation to avoid unnecessary straining and further injury to the sphincter muscles
biofeedback
356
3 main hemorrhoidal complexes
left lateral
right anterior
right posterior
357
diagnostic technique to identify position of hemorrhoidal disease
anoscopy
358
description of stage I hemorrhoid
enlargement with bleeding
359
description of stage II hemorrhoid
protrusion with spontaneous reduction
360
description for Stage III hemorrhoids
protrusion requiring manual reduction
361
description of stage IV hemorrhoid
irreducible protrusion
362
managemnet for acutely thrombosed hemorrhoid
excision within 1st 72 hours
363
results from an infection involving the glands surrounding the anal canal
anorectal abscess
364
most common location opf anorectal abscess
perianal (40-50%)
other locations:
ischiorectal - 20-25%
intersphincteric - 2-5%
supralevator - 2.5%
365
hallmarks of anorectal abscess (2)
pain and fever
366
T or F: all patients with anorectal abscess must be treated with antibiotics
false
only those who are immunocompromised, have prosthetic hearrt valves, artificial joints or IBD
367
origin of the majority of fistula in ano
cryptoglandular
368
communication of an abscess cavity with an identifiable internal opening within the anal canal
fistula in ano
369
fistula in ano most commonly opens in
dentate line (where anal glands enter anal canal
370
most commpon fistula in ano based on the relation to the anal sphincter muscles
intersphincteric - 70%
transphincteric - 23%
suprasphincteric - 5%
extrasphincteric - 2%
371
presents as constant drainage from perianal region associated with a firm mass and increasing with defecation
fistula in ano
372
A posterior external fistula will enter the anal canal in the posterior midline, whereas an anterior fistula will enter the nearest crypt. this is called the
Goodsall's rule
exception to this rule: if exiting > 3 cm from anal verge
373
best option of treatment for new cases of fistula in ano
placement of seton (vessel loop or silk tie placed through the fistula tract)
374
Surgical tretament for intersphincteric and low transphincteric fistula in ano:
siimple fistulotomy
375
surgical treatment for high transsphincteric fistula in ano
anorectal advancement flap in combination with drainage catheter or fibrin glue
376
Anal fissure commonly involves which part of the anal canal?
posterior anal cancal
but also involves the anterior
377
Suspected causes for anal fissure not located at the posterior or anterior anal fissure (4)
TB
syphilis
Crohn's
CA
378
pathognomonic findings of anal fissure on anal manometry
increased anal resting pressure + sawtooth deformity with paradoxical contractions of the sphincter muscles
379
duration of chronic anal fissures
> 6 weeks
380
occurs when splanchnic perfusion fails to meet the metabolic demands of the intestines
intestinal ischemia secondary to ischemic tissue injury
381
Intestinal ischemia is classified based on etiology, which dictates management. These are (3):
(1) arterioocclusive mesenteric ischemia
(2) non-occlusive mesenteric ischemia
(3) mesenteric venous thrombosis
382
Risk factors for arterioocclusive mesenteric ischemia (4):
Atrial fibrillation
Recent myocardial infarction
Valvular heart disease
Recent cardiac or vascular catheterization
All of which are acute in onset and result in embolic clots reaching the mesenteric circulation
383
A class of intestinal ischemia also known as “intestinal angina,” that is generally more insidious and often seen in the aging population affected by atherosclerotic disease
Nonocclusive mesenteric ischemia
384
Causes of nonocclusive mesenteric ischemia (4)
Atherosclerotic disease
High-dose vasopressor infusions
Patients presenting with cardiogenic or septic shock,
Cocaine overdose
385
It is the most prevalent gastrointestinal disease complicating cardiovascular surgery.
Nonocclusive mesenteric ischemia
386
The incidence of ischemic colitis following elective aortic repair is
5–9%, and the incidence triples in patients following emergent repair
387
Risk factor for mesenteric venous thrombosis
hypercoagulable state
388
Collateral vessels within the small bowel are numerous and meet within the duodenum and the bed of the pancreas. This area is known as:
Griffiths’ point
389
Collateral vessels within the colon meet at the splenic flexure and descending/sigmoid colon. This area is known as:
Sudeck’s point
390
2 areas that are inherently at risk for decreased blood flow that may cause intestinal ischemia
Griffiths’ point and Sudeck’s point
391
the most common locations for colonic ischemia (2)
Griffiths’ point and Sudeck’s point
392
The splanchnic circulation can receive up to ___ of the cardiac output.
30%
393
Protective responses to prevent intestinal ischemia include (3)
Abundant collateralization
Autoregulation of blood flow
Ability to increase oxygen extraction from the blood
394
Most frequent origin of emboli that cause intestinal ischemia
Heart (in 75% of cases)
395
In intestinal ischemia, where does the emboli preferentially lodge?
superior mesenteric artery (SMA) just distal to the origin of the middle colic artery
396
T or F: Progressive thrombosis of at least 3 of the major vessels supplying the intestine is required for the development of chronic intestinal angina
false. 2
397
A disproportionate mesenteric vasoconstriction (arteriolar vasospasm) in response to a severe physiologic stress such as shock
Nonocclusive ischemia
398
Mortality rate of intestinal ischemia
>50%
399
The most significant indicator of survival in intestinal ischemia
timeliness of diagnosis and treatment
400
Presents with severe acute, nonremitting abdominal pain strikingly out of proportion to the physical findings, associated with nausea and vomiting, transient diarrhea, anorexia, and bloody stools
Acute mesenteric ischemia
401
PE finding of early acute mesenteric ischemia (2)
minimal abdominal distention and hypoactive bowel sounds
The rest is normal
402
Later findings in acute mesenteric ischemia (2)
peritonitis and cardiovascular collapse
403
T or F: Diagnostic modalities are useful in diagnosis of intestinal ischemia but should not delay surgical therapy
True
404
Earlier features of this disease seen on abdominal radiographs include bowel-wall edema, known as “thumbprinting.”
intestinal ischemia
405
Progression of this disease will have the radiographic findings of air seen within the bowel wall (pneumatosis intestinalis) and within the portal venous system.
intestinal ischemia
406
A highly sensitive test for intestinal ischemia
CT angiography with three-dimensional reconstruction
407
In acute embolic disease causing intestinal ischemia, this test is best performed intraoperatively
mesenteric angiography
408
T or F: A negative duplex scan does not exclude the diagnosis of mesenteric ischemia
False, virtually precludes the diagnosis
409
One of the biggest limitations of duplex scanning is
Patients’ body habitus
The duplex imaging yields poor results in obese patients
410
When suspecting mesenteric ischemia involving the colon, performing this test is high yield. This is often an excellent diagnostic tool in patients with chronic renal insufficiency who cannot tolerate IV contrast.
endoscopy
411
The “gold standard” for the diagnosis of acute arterial occlusive disease is
Angiography
412
The “gold standard” for the management of acute arterial occlusive disease is
laparotomy
413
The goal of operative exploration in intestinal ischemia is to
resect compromised bowel and restore blood supply
414
Site of occlusion when the proximal jejunum is often spared while the remainder of the small bowel up to the transverse colon will be ischemic.
SMA
415
The surgical management of acute mesenteric ischemia of the small bowel is
embolectomy via arteriotomy
416
The presence of these laboratory results are useful in support of the diagnosis of advanced intestinal ischemia (4)
Leukocytosis
Metabolic acidosis
Elevated amylase or creatinine phosphokinase levels
Lactic acidosis
these markers may not be indicative of either reversible ischemia or frank necrosis
417
Investigational markers for intestinal ischemia include (4)
d-dimer
glutathione S-transferase
platelet- activating factor (PAF)
mucosal pH monitoring
418
Why do we need aggressive fluid resuscitation in intestinal ischemia?
Early manifestations of intestinal ischemia include fluid sequestration within the bowel wall leading to a loss of interstitial volume.
419
Intervention of choice to maintain hemodynamics in intestinal ischemia
fluid resuscitation
420
Ischemia of the colonic mucosa is graded as mild, moderate and severe. Describe each.
Mild - minimal mucosal erythema
Moderate - pale mucosal ulcerations and evidence of extension to the muscular layer of the bowel wall
Severe - severe ulcerations resulting in black or green discoloration of the mucosa, consistent with full-thickness bowel-wall necrosis
421
Degree of reversibility of mild, moderate, and severe ischemia of colonic mucosa
mild - nearly 100%
moderate - ~50%
frank necrosis - dead bowel
422
T or F: Primary anastomosis may be performed in patients with acute intestinal ischemia
False
423
The diagnosis of mesenteric thrombosis is frequently made on
abdominal spiral CT with oral and IV contrast
424
The goal of management of mesenteric venous thrombosis are (4)
optimize hemodynamics
correct electrolyte abnormalities with massive fluid resuscitation
Intravenous antibiotics
anticoagulation
425
Of all acute intestinal disorders, this is associated with the best prognosis.
Mesenteric venous insufficiency
426
Presents with intestinal angina, post-prandial abdominal pain, weight loss and chronic diarrhea
Chronic intestinal ischemia
associated with increased need of blood flow to the intestine following meals - hence the post prandial pain
427
T or F: Abdominal pain without weight loss is not chronic mesenteric angina
True
428
The treatment of chronic mesenteric ischemia is associated with an 80% long-term success rate
Angioplasty with endovascular stenting
429
Main stimulator of secretion of water and electrolytes from the pancreatic ductal cells
Secretin (lesser extent, CCK)
430
Evokes an enzyme-rich secretion from pancreatic acinar cells
CCK
431
5 causes of acute pancreatitis
Gallstone, alcohol, ERCP, hypertriglyceridemia, drugs
432
Type of pancreatitis where pancreas blood supply is maintained
Interstitial pancreatitis
433
Type of pancreatitis where pancreas blood supply is interrupted
Necrotizing pancreatitis
434
Accepted pathogenic theory of acute pancreatitis where proteolytic enzymes are activated in the pancreas acinar cell rather than in the intestinal lumen due to premature activation of trypsin
Autodigestion
435
Major symptom of acute pancreatitis
Abdominal pain
436
Characteristic of abdominal pain in acute pancreatitis
Steady and boring in the epigastrium or periumbilical region, and may radiate to the back, chest, flanks, and lower abdomen
437
3 causes of shock in acute pancreatitis
o Hypovolemia
o Increased kinin peptides – causing vasodilation
o Systemic effects of proteolytic and lipolytic enzymes
438
Part of pancreas that is edematous when there is occurrence of jaundice
Head of the pancreas
439
Location of pleural effusion in acute pancreatitis
Left-sided
440
Faint blue discoloration around the umbilicus
Cullen’s sign
441
Cause of cullen’s sign
Hemoperitoneum
442
Blue-red-purple or green-brown discoloration of the flanks
Turner’s sign
443
Cause of Turner’s sign
Due to tissue catabolism of hemoglobin from severe necrotizing pancreatitis with hemorrhage
444
Serum amylase in acute pancreatitis returns to normal in how many days:
3-7 days
445
Serum lipase in acute pancreatitis returns to normal in how many days
7-14 days
446
Preferred test for acute pancreatitis
Lipase
447
More specific test for acute pancreatitis
Lipase
448
Harbinger of more severe disease (i.e. pancreatic necrosis) in acute pancreatitis
Hemoconcentration (Hct > 44%)
449
Cause of prerenal azotemia in acute pancreatitis
Due to loss of plasma intro the retroperitoneal space and peritoneal cavity
450
3 causes of hyperglycemia in acute pancreatitis:
o Decreased insulin release
o Increased glucagon release
o Increased output of adrenal glucocorticoids and catecholamines
451
Elevated ALP, AST and bilirubins in acute pancreatitis indicates involvement of:
Gallbladder and pancreatic head
452
Initial diagnostic imaging modality in acute pancreatitis
Abdominal ultrasound
453
Criteria that categorized morphologic features of acute pancreatitis via CT scan:
Revised atlanta criteria
454
3 criteria for acute pancreatitis diagnosis (2 out 3)
o Typical abdominal pain in the epigastrium that may radiate to the back
o 3-fold or greater elevation in serum lipase and/or amylase
o Confirmatory findings of acute pancreatitis on cross-sectional abdominal imaging
455
4 markers of severity of acute pancreatitis
o Hemoconcentration (Hct > 44%)
o Admission azotemia (BUN > 22 mg/dL)
o SIRS
o Signs of organ failure
456
2 Differences between the biliary colic and acute pancreatitis abdominal pain
o Pain of biliary tract origin is more-right sided or epigastric than umbilical or left upper quadrant
o Ileus is usually absent
457
Criteria that defines phases of acute pancreatitis, outlines severity of acute pancreatitis, and clarifies imaging definition
Revised Atlanta criteria
458
2 phases of acute pancreatitis
o Early < 2 weeks
| o Late > 2 weeks
459
Phase of acute pancreatitis where Severity is defined by clinical parameters rather than morphologic findings
Early phase
460
Most important clinical finding in regard to severity of the acute pancreatitis episode
Persistent organ failure – > 48 h
461
You must do CT imaging in the 1st 48 h of admission of acute pancreatitis: true or false
False
462
Radiographic feature of greatest importance to recognize in the late phase of acute pancreatitis
Necrotizing pancreatitis of CT
463
Difference between moderately severe and severe acute pancreatitis
o Moderately severe – transient organ failure (<48h)
| o Severe – persistent organ failure (>48h)
464
Diffuse pancreatic enlargement and homogenous contrast enhancement on CT scan
Interstitial pancreatitis
465
Lack of pancreatic parenchymal enhancement by IV contrast on CT scan
Necrotizing pancreatitis
466
Most important treatment intervention for acute pancreatitis
Safe, aggressive IV fluid resuscitation
467
Better crystalloid for hydration in acute pancreatitis
Lactated Ringer’s
468
What is safe, aggressive IV fluid resuscitation in acute pancreatitis
15-20 ml/kg (1050-1400) mL as initial bolus followed by 2-3 ml/kg/hr (200-250 mL/h) to maintain UO > 0.5 ml/kg/hr
469
Why is Lactated Ringer’s solution a better crystalloid than NSS?
Decrease systemic inflammation
470
Strategy wherein there is measurement of hematocrit and BUN every 8-12 hrs to ensure adequacy of fluid resuscitation
Targeted resuscitation strategy
471
5 clinical and laboratory parameters in BISAP
```
o BUN > 25 mg/dL
o Impaired mental status (GCS < 15)
o SIRS
o Age > 60 years
o Pleural effusion
```
472
BISAP score that indicates increased risk for in-hospital mortality
≥ 3
473
Diet for mild acute pancreatitis (once abdominal pain resolved)
Low-fat solid diet
474
Preferred nutrition for more severe cases after 2-3 days of admission
Enteral nutrition (preferred than TPN)
475
Prophylactic antibiotics is recommended for necrotizing pancreatitis: True or false
False; broad spectrum antibiotic may be given if patient appears septic, then discontinued once with negative cultures
476
Definitive management of infected pancreatic necrosis
Pancreatic debridement (necrosectomy)
477
Persistent pancreatic fluid collections after 6 weeks
Pseudocyst
478
Diagnosis of pancreatic duct disruption is confirmed by what diagnostic?
MRCP or ERCP
479
> 90% effective at resolving the leak in pancreatic duct disruption
Bridging pancreatic stent (nonbridging are less effective)
480
3 perivascular complications of acute pancreatitis:
o Splenic vein thrombosis
o Gastric varices
o Pseudoaneurysm
481
Incidence of recurrent pancreatitis
25% of patients
482
2 most common etiologic factors of recurrent pancreatitis
o Alcohol
| o Cholelithiasis
483
4 Cardinal manifestations of chronic pancreatitis
o Abdominal pain
o Steatorrhea
o Weight loss
o Diabetes mellitus
484
Primary cause of chronic pancreatitis
Alcohol
485
Independent, dose-dependent risk factor for chronic pancreatitis and recurrent acute pancreatitis
Smoking
486
Most frequent cause of chronic pancreatitis in children
Cystic fibrosis
487
Pancreatitis that has the following histopathologic findings: Lymphoplasmacytic infiltrate, storiform fibrosis, abundant IgG4 cells
Autoimmune pancreatitis
488
Marker for autoimmune pancreatitis
IgG4 – elevated in 2/3 of patients
489
Criteria used in diagnosing autoimmune pancreatitis
Mayo Clinic HISORt criteria
490
Parameters in Mayo Clinic HISORt criteria for AIP
```
o At least 1 or more of the following:
Histology
Imaging
Serology
Other organ involvement
Response to glucocorticoid therapy
```
491
Treatment of AIP that has dramatic response within 2- to 4-week course
Glucocorticoids
492
Dose of prednisone in AIP
o Initial dose: 40 mg/day for 4 weeks
| o Tapered by 5 mg/week
493
Very effective at inducing and maintaining remission in AIP
Rituximab
494
In chronic pancreatitis, patients seek medical attention predominantly because of 2 symptoms. What are these?
o Abdominal pain or maldigestion
| o Weight loss
495
2 tests used in evaluation of suspected pancreatic steatorrhea
o Fecal-elastase-1 – abnormal (low)
| o Small bowel biopsy – normal
496
Initial modality of choice in chronic pancreatitis
Abdominal CT imaging
497
Test that has best sensitivity and specificity in chronic pancreatitis
Hormone stimulation test using secretin
498
Radiographic findings that is pathognomonic for chronic pancreatitis
Diffuse calcifications on plain films
499
Arterial bleeding into the pancreatic duct
Hemosuccus pancreaticus
500
The cumulative risk of pancreatic carcinoma in chronic pancretitis
4% after 20 years
501
Cornerstone of therapy in pancreatic steatorrhea
Pancreatic enzyme replacement
502
Pancreatic enzyme replacement formulation must deliver sufficient amount of what substance into the duodenum to correct maldigestion and decrease steatorrhea?
Lipase
503
Hereditary pancreatitis is mutation on gene on what chromosome? What codons?
Chromosome 7, codons 29 and 122
504
Incidence of pancreatic carcinoma in hereditary pancreatitis at age 70
40%
505
Ventral pancreatic anlage fails to migrate correctly to make contact with the dorsal anlage
Annular pancreas
506
Ring of pancreatic tissue encircling the duodenum
Annular pancreas
507
Surgical procedure of choice for annular pancreas
Retrocolic duodenojejunostomy
508
Most common congenital anatomic variant of human pancreas
Pancreas divisum
509
Pancreas divisum does not predispose patients to pancreatitis: True or false
True
510
Appear as a small-caliber ventral duct with an arborizing pattern on ERCP/MRCP
Pancreas divisum
511
Treatment of pancreatitis with pancreas divisum
o Conservative
| o Endoscopic or surgical intervention only if with recurrence
512
Diagnostic test for macroamylasemia
Serum chromatography
513
Amylase circulate in the blood in a polymer form too large to be easily excreted by the kidney
Macroamylasemia
514
Most common cause of UGIB
Peptic ulcers
515
3 high risk findings of ulcer on endoscopy
* Active bleeding
* Nonbleeding visible vessel
* Adherent clot
516
High-dose, constant infusion of IV PPI sustain intragastric pH of:
> 6
517
Rebleeding percentage of peptic ulcers within the next year if no preventive strategies done
10-50%
518
3 main factors in ulcer pathogenesis:
* Helicobacter pylori
* NSAIDs
* Acid
519
Eradication of H. pylori decrease PUD rebleeding to:
< 5%
520
If necessary, what NSAID would you give in patient with GIB?
COX-2 selective plus a PPI
521
For GIB patients with CVD who takes low-dose aspirin for secondary prevention, when will you resume aspirin?
Restart aspirin ASAP after their bleeding episode (1-7 days)
522
For GIB patients who take aspirin for primary prevention, when will you resume aspirin?
No need to resume
523
If GIB is unrelated to H. pylori or NSAIDS, until when should you give PPI to patients?
Should remain on PPI therapy indefinitely because of rebleeding rates of 42% at 7 years
524
Most common bleeding site of Mallory-Weiss tear
Gastric side of the GEJ
525
Mallory-Weiss tear stops spontaneously in how many percent of cases?
80-90%
526
Recurrence rate of Mallory-Weiss Tear
0-10%
527
Poorer outcomes than other sources of UGIB
Esophageal varices
528
4 treatment for Esophageal varices
* Endoscopic ligation
* IV vasoactive medications
* Non-selective beta blockers
* TIPS
529
2 indications of TIPS in patient with BEV:
* For patients with persistent or recurrent bleeding despite endoscopic and medical therapy
* 1st 1-2 days of hospitalization for acute BEV in patients with advanced liver disease (Child-Pugh class C with score 10-13)
530
Endoscopically visualized breaks that are confined to the mucosa
Erosive disease
531
Cause of erosive esophagitis
GERD
532
Most important cause of gastric and duodenal erosions
NSAID use
533
Watermelon stomach
Gastric antral vascular ectasia
534
Aberrant vessel in mucosa bleeds from a pinpoint mucosal defect
Dieulafoy’s lesion
535
Hereditary hemorrhagic telangiectasias
Osler-Weber-Rendu
536
Prolapse of proximal stomach into esophagus with retching
Prolapse gastropathy
537
Bleeding from the bile duct
Hemobilia
538
Bleeding from pancreatic duct
Hemosucus pancreaticus
539
Percentage of obscure GIB that originate in the small intestine
~75%
540
3 most common causes of small-intestinal GIB in >40 years old:
* Vascular ectasias
* Neoplasm
* NSAID-induced erosions and ulcers
541
Most common cause of significant small intestinal GIB in children
Meckel diverticulum
542
Most common cause of LGIB
Hemorrhoids
543
Aside from hemorrhoids and anal fissures, what is the most common cause of LGIB?
Diverticulosis
544
Usual location of diverticulosis
Right colon
545
Bleeding stop spontaneously in how many percent of diverticulosis?
~80-90%
546
Rebleeding rate in diverticulosis
~15-40%
547
Without source of GIB identified on UGIE and colonoscopy
Obscure GIB
548
Bleeding vascular ectasias and aortic stenosis
Heyde’s syndrome
549
2 most common causes of significant colonic GIB in children and adolescents
* Inflammatory bowel disease
| * Juvenile polyps
550
Measurement of these 2 is the best way to initially assess a patient with GIB
Heart rate and BP
551
It may take up to how many hours for Hgb to fall in acute GIB
72 hrs
552
Hemoglobin does not fall immediately in acute GIB. Why?
Proportionate reductions in plasma and red cell volumes
553
Transfusion is recommended once Hgb is _____. And what do you call this strategy?
* ≤ 7 g/dL
| * Restrictive transfusion strategy
554
In melena, blood has been present in the GIT for how many hours?
≥ 14 h or as long as 3-5 days
555
Aside from melena, what are 2 other clues of UGIB in differentiating with LGIB?
* Hyperactive bowel sounds
| * Elevated BUN
556
3 baseline characteristics predictive of rebleeding and death in UGIB:
* Hemodynamic compromise
* Increasing age
* Comorbidities
557
Promotility agent to improve visualization? Dose?
Erythromycin 250 mg IV ~ 30 min before endoscopy
558
In what subset of UGIB patients will you give antibiotics? And what antibiotics?
* Cirrhotic
| * Quinolone or ceftraixone
559
May improve control of bleeding in cirrhotics with UGIB in the 1st 12 h after presentation
IV vasoactive medications
560
When should you perform upper endoscopy? In high-risk patients?
* Within 24 hrs
| * Within 12 hrs
561
BUN scoring in Glasgow- Blatchford score
* 18.2 to <22.4 = 2
* 22.4 to <28.0 = 3
* 28.0 to <70.0 = 4
* ≥ 70 = 6
562
Hemoglobin scoring in Glasgow- Blatchford score (men and women)
* 12 to <13 (men) = 1
* 10 to <12 (women) = 1
* 10 to <12 (men = 3
* <10 = 6
563
SBP scoring in Glasgow- Blatchford score
* 100-109 = 1
* 90-99 = 2
* <90 = 3
564
Heart rate scoring in Glasgow- Blatchford score
≥ 100 = 1
565
Scoring of other markers in Glasgow- Blatchford score
* Melena = 1
* Syncope = 2
* Hepatic disease = 2
* Cardiac failure = 2
566
In patients with hematochezia + hemodynamic instability, what procedure should you do first?
UGIE to rule out UGIB
567
Procedure of choice for LGIB, unless bleeding is too massive
Colonoscopy
568
Procedure for massive LGIB
Angiography
569
Procedure for LGIB in patients < 40 years old with minor bleeding
Sigmoidoscopy
570
Initial test in patients with massive bleeding from the small intestine
Angiography
571
Next step in patients with GIB with negative UGIE or colonoscopy
* Second-look procedure – repeat upper and lower endoscopy
| * May also do push enteroscopy
572
Inspect the entire duodenum and proximal jejunum with a pediatric colonoscope
Push enteroscopy
573
If second-look procedure in GIB patient is negative, what is the next step?
Video capsule endoscopy (may also do push enteroscopy)
574
May be used initially instead of video capsule in patients with possible small bowel narrowing
CT enterography
575
If capsule endoscopy is negative, what is the next step?
Observe or do further testing with deep enteroscopy
576
Next step if you have a positive FOBT:
Do colonoscopy
577
Responsible for nearly 50% of the mortality from all cirrhosis
Chronic and excessive alcohol ingestion
578
Pathology of ALD consists of three major lesions:
Fatty liver
Alcoholic hepatitis
Cirrhosis
579
Mortality of patients with alcoholic hepatitis concurrent with cirrhosis:
nearly 60% at 4 years
580
World's third largest risk factor for disease burden
Alcohol
581
Cause of most of the mortality attributed to alcohol
Cirrhosis
Mortality is directly related to alcohol consumption
582
The most important risk factors involved in the development of ALD (2)
Quantity and duration of alcohol intake
583
T or F. Men are more susceptible to ALD
False. Women are more susceptible.
* Develop advanced liver disease with substantially less alcohol intake
* Due to effects of estrogen, proportion of body fat, and gastric metabolism of alcohol
584
~12g of alcohol is equivalent to (in terms of beer, wine and spirits)?
* 1 beer
* 4 oz of wine
* 1 oz of 80% spirits
585
Threshold in developing ALD (women and men)
* >14 drinks per week in men
| * > 7 drinks per week in women
586
Beverage that has protective effect in ALD
Coffee
587
The initial and most common histologic response to hepatotoxic stimuli
Fatty liver
588
The major enzyme responsible for alcohol metabolism
alcohol dehydrogenase
589
Hepatocyte injury characterized by: ballooning degeneration, spotty necrosis, polymorphonuclear infiltrate, and fibrosis in the perivenular and perisinusoidal space of Disse
Alcoholic hepatitis
590
Critically ill patients with alcoholic hepatitis short-term (30-day) mortality rates of >50% is seen in patients with (6)
* Coagulopathy – prothrombin time increased >5 s
* Anemia
* Serum albumin <25 g/L (2.5 mg/dL)
* Serum bilirubin >137 μmol/L (8 mg/dL)
* Renal failure
* Ascites
591
In liver disease, discriminant function score that indicates poor prognosis is
>32
592
Model for End-Stage Liver Disease (MELD) score that indicates significant mortality in alcoholic hepatitis
≥21
593
Based on MELD scoring, dismal prognosis of cirrhosis is seen in patients with (4)
* Ascites
* Variceal hemorrhage
* Deep encephalopathy
* Hepatorenal syndrome
594
the cornerstone in the treatment of alcoholic liver disease
Complete abstinence from alcohol
595
Glucocorticoids may be given in ALD if the DF is ___ and MELD scores is ____
For DF >32 or MELD >20
Prednisone 40 mg/day or Prednisolone 32 mg/day for 4 weeks
596
T or F. Women with encephalopathy from severe alcoholic hepatitis are good candidates for glucocorticoids
True
597
Nonspecific TNF inhibitor that may be used for severe alcoholic hepatitis
Pentoxifylline
598
T or F. Transplant candidacy for ALD should be reevaluated after a defined period of sobriety
Patients presenting with alcoholic hepatitis – not a transplant candidate
599
In men, ______ of ethanol produces fatty liver; ______ for 10–20 years causes hepatitis or cirrhosis. Only ____ of alcoholics develop alcoholic liver disease.
40–80 g/d
160 g/d
15%
600
T or F. When the underlying insult that has caused the cirrhosis has been removed, there can be reversal of fibrosis
True
601
Reversal of fibrosis is most apparent in treatment of what cause of cirrhosis?
chronic hepatitis C
602
Reversal of fibrosis may be observed after treatment of what underlying causes of cirrhosis? (3)
* Chronic hepatitis C
* Hemochromatosis
* Alcoholic liver disease
603
In terms of nodules, alcoholic cirrhosis is classified as
Micronodular cirrhosis
Nodules are usually < 3 mm in diameter
604
In terms of nodules, alcoholic cirrhosis after cessation of alcohol use is classified as
mixed macro- and micronodular cirrhosis
larger nodules may form after cessation
605
Ethanol is mainly absorbed by the
small intestine and through stomach (lesser degree)
606
Unique form of hemolytic anemia in severe alcoholic hepatitis with spur cells and acanthocytes
Zieve’s syndrome
607
Reflective of portal hypertension with hypersplenism in cirrhosis
Thrombocytopenia
608
AST:ALT ration in alcoholic cirrhosis
2:1
609
Liver biopsy is withheld until abstinence has been maintained for at least
6 months to determine residual, nonreversible disease
610
5-year survival rate for patients with complications of cirrhosis and continue to drink
<50%
611
Cornerstone of therapy of alcoholic cirrhosis
Abstinence
612
Percentage of hepatitis C virus that develop into chronic hepatitis C
80%
613
Percentage of chronic hepatitis C will develop cirrhosis over 20-30 years
20-30%
614
T or F. Liver damage in cirrhosis secondary to chronic hepatitis C is due to cytopathic effect of the virus
False. It is a noncytopathic virus – liver damage is probably immune-related
615
In terms of nodules, cirrhosis secondary to chronic hepatitis C is classified as
mixed macro- and micronodular cirrhosis
616
Percentage of hepatitis B virus that develop into chronic hepatitis B
5%
617
Percentage of chronic hepatitis B will develop cirrhosis
20%
618
Highly successful therapy for cirrhosis with hepatitis C
Direct-acting antiviral protocols
* Well-tolerated
* Short duration (8-12 weeks)
* Costly
619
T or F. Treatment of autoimmune hepatitis includes immunosuppressive therapy such as glucocorticoids or azathioprine
False. Will not benefit from immunosuppressive therapy with glucocorticoids or azathioprine because the AIH is “burned out”.
620
Positive autoimmune markers in autoimmune hepatitis (2)
* ANA
| * Anti-smooth-muscle antibody (ASMA)
621
T or F. Non-alcoholic steatohepatitis can progress to increased fibrosis and cirrhosis
True
622
Type of biliary cirrhosis that will have no improvement with surgical or endoscopic interventions
Intrahepatic
623
Type of biliary cirrhosis that will benefit from surgical or endoscopic biliary tract decompression
Extrahepatic
624
All chronic cholestatic syndromes share the histopathologic features of chronic cholestasis, such as (4)
* Cholate stasis
* Copper deposition
* Xanthomatous transformation of hepatocytes
* Irregular biliary fibrosis
625
Major causes of chronic cholestatic syndromes (4)
* Primary biliary cholangitis
* Autoimmune cholangitis
* Primary sclerosing cholangitis
* Idiopathic adulthood ductopenia
626
T or F. Primary biliary cholangitis has strong male preponderance.
False. Female
Mostly seen in middle-aged women
627
Portal inflammation and necrosis of cholangiocytes in small- and medium-sized bile ducts
Primary biliary cholangitis
628
Antibodies present in 90% of cases of primary biliary cholangitis
Antimitochondrial antibodies (AMA)
* Not pathogenic
* Useful markers for making a diagnosis of PBC
629
Treatment of primary biliary cholangitis (3)
1. Liver transplantation
2. Ursodeoxycholic acid (UDCA)
3. Obeticholic acid
630
Treatment of choice for primary biliary cholangitis patients with decompensated cirrhosis
Liver transplantation
631
The only approved treatment that has some degree of efficacy by slowing the rate of progression of the primary biliary cholangitis
Ursodeoxycholic acid (UDCA)
13-15 mg/kg/day
Slow the rate of progression of PBC, but it does not reverse or cure the disease
632
Approved for use in primary biliary cholangitis patients with inadequate response to UDCA
Obeticholic acid
633
Earliest lesion of primary biliary cholangitis
Chronic nonsuppurative destructive cholangitis
* Necrotizing inflammatory process of the portal tracts
* Medium and small bile ducts are infiltrated with lymphocytes and undergo duct destruction
634
In terms of nodules, cirrhosis secondary to primary biliary cholangitis is classified as
Micro- or macronodular
635
Most notable clinical feature of primary biliary cholangitis
Significant degree of fatigue out of proportion to what be expected for either severity of the liver disease or the age of the patient
636
The presence of this symptom prior to the development of jaundice indicates severe disease and poor prognosis
Pruritus
Present in 50% of cases and can be debilitating
637
Features that are unique to primary biliary cholangitis (3)
1. Hyperpigmentation (trunk and arms; seen in areas of exfoliation and lichenification associated with progressive scratching)
2. Xanthelasma
3. Xanthomata
638
This tests are most important in the setting of AMA-negative PBC (2)
1. Liver biopsy
| 2. Cholangiography
639
Cholangiography must be done in patients with AMA-negative with cholestatic liver enzymes to rule out
Primary sclerosing cholangitis
640
Treatment for intractable pruritus in PBC
Plasmapheresis
641
Chronic cholestatic syndrome characterized by diffuse inflammation and fibrosis involving the entire biliary tree
Primary sclerosing cholangitis
642
Final, end-stage manifestation of PSC
Biliary cirrhosis
643
Biopsy finding in PSC
periductal fibrosis
Helpful in making diagnosis
644
Antibodies that is positive in 65% of PSC
pANCA
645
GI condition that is present in > 50% of patients with PSC
Ulcerative colitis
646
Colonoscopy must be performed once PSC is established to rule out
Ulcerative colitis
647
Definitive diagnostic test for PSC
Cholangiography
648
Imaging technique of choice for initial evaluation of PSC
MRCP
649
ERCP is performed in PSC to determine presence of
dominant stricture
650
Cholangiographic findings of multifocal stricturing and beading involving both the intra- and extrahepatic biliary tree (classic beaded appearance)
Primary sclerosing cholangitis
Stricture is short and with intervening segments of normal or slightly dilated bile ducts that are distributed diffusely
651
PSC appearance on cholangiography associated with overall poor prognosis
High-grade, diffuse structuring of the intrahepatic bile ducts
652
Definitive treatment of PSC
Liver transplantation
653
Dreaded complication of PSC
Cholangiocarcinoma
Relative contraindication for liver transplantation
654
Cardiac cirrhosis is secondary to
long-standing right-sided CHF
655
Description of fibrosis in cardiac cirrhosis
Pericentral
656
Inherited disorder of iron metabolism with progressive increase in hepatic iron deposition
Hemochromatosis
657
Treatment of hemochromatosis
regular therapeutic phlebotomy
658
Inherited disorder of copper homeostasis causing failure in excretion of excess amounts of copper resulting to accumulation of copper in the liver
Wilson’s disease
659
Kayser-Fleischer corneal rings is seen in
Wilson’s disease
660
Low ceruloplasmin and elevated 24-h urine copper levels are seen in
Wilson’s disease
661
Treatment of Wilson’s disease
copper-chelating medications
662
inherited disorder that causes abnormal folding of the α1AT protein
α1AT deficiency
663
α1AT deficiency phenotype with greatest risk for development of chronic liver disease
ZZ phenotype
Only 10-20% develops chronic liver disease
664
Liver biopsy result of periodic acid-Schiff (PAS)-positive and diastase-resistant globules
α1AT deficiency
665
Only effective treatment in α1AT deficiency
Liver transplantation
666
Portal hypertension is elevation of the hepatic venous pressure gradient (HVPG) to
> 5 mmHg
667
Portal hypertension is caused by 2 simultaneously occurring hemodynamic processes:
1. Increased intrahepatic resistance to the passage of blood flow through the liver due to cirrhosis and regenerative nodules
2. Increased splanchnic blood flow secondary to vasodilation within the splanchnic vascular bed
668
Portal hypertension is directly responsible for 2 major complications of cirrhosis
1. Variceal hemorrhage
| 2. Ascites
669
Mortality rate of BEV with each episode of bleeding
20-30%
670
Prehepatic causes of portal hypertension (3)
1. Portal vein thrombosis
2. Splenic vein thrombosis
3. Massive splenomegaly (Banti’s syndrome)
671
Which is the most common cause of portal hypertension: pre, intra, or posthepatic?
Intrahepatic (95%)
presinusoidal, sinusoidal, or postsinusoidal
672
Cirrhosis is presinusoidal, sinusoidal, or postsinusoidal cause of portal hypertension?
Sinusoidal
673
Presinusoidal cause of portal hypertension (2)
1. Congenital hepatic fibrosis
| 2. Schistosomiasis
674
Percentage of cirrhotic patients that has portal HPN
>60%
675
Postsinusoidal cause of portal hypertension
Venoocclusive disease
676
Posthepatic causes of portal hypertension (3)
1. Budd-Chiari Syndrome
2. Venoocclusive disease
3. Chronic right-sided cardiac congestion
Affecting the hepatic veins and venous drainage to the heart
677
3 primary complications of portal hypertension
1. Gastroesophageal varices with hemorrhage
2. Ascites
3. Hypersplenism
678
Hepatic venous pressure gradient (HVPG) that is at risk for variceal hemorrhage
> 12 mmHg
679
Sinusoidal cause of portal hypertension (2)
1. Cirrhosis
| 2. Alcoholic hepatitis
680
____ of patients with cirrhosis have varices. And ____ of patients with varices will develop bleeding
1/3
| 1/3
681
_____ of cirrhotics per year develop varices
5-15%
682
Certain endoscopic stigmata for esophageal varices (6)
1. Red wale sign
2. Hematocystic spots
3. Diffuse erythema
4. Bluish color
5. Cherry red spots
6. White-nipple spots
683
2 main categories of treatment of esophageal varices
1. Primary prophylaxis
| 2. Prevention of rebleeding
684
Primary prophylaxis of esophageal varices (3)
1. Endoscopy for routine screening
2. Nonselective beta blockade (Nadolol and propranolol)
3. Endoscopic variceal band ligation
685
Medications that decrease mortality related to variceal hemorrhage
Nonselective beta blockade (Nadolol and propranolol)
686
Prevention of rebleeding in esophageal varices is achieved by
Repeated variceal band ligation until varices are obliterated
687
Vasoconstricting agents used in BEV (3)
Somatostatin
Octreotide
Vasopressin
688
A direct splanchnic vasoconstrictor given in BEV
Octreotide 50-100 μg/h by continuous infusion
689
Treatment of acute BEV for patients who cannot get endoscopic therapy immediately or who need stabilization prior to endoscopic therapy
Balloon tamponade
• Sengstaken-Blakemore tube
• Minnesota tube
690
First-line treatment to control bleeding acutely in BEV
Endoscopic intervention
Sclerotherapy
EVBL
691
If with bleeding from gastric varices that cannot be controlled by EVL, what is the next step?
Transjugular intrahepatic portosystemic shunt (TIPS)
Creates a portosystemic shunt by a percutaneous approach using an expandable metal stent, which is advanced under angiographic guidance to the hepatic veins and then through the substance of the liver to create a direct portocaval shunt
692
Alternative to surgery for acute decompression of portal hypertension
Transjugular intrahepatic portosystemic shunt (TIPS)
693
Complication of TIPS (in 20% of patients)
Encephalopathy
694
Reserved for BEV patients who fail endoscopic or medical management or who are poor surgical risks
Transjugular intrahepatic portosystemic shunt (TIPS)
695
Management of recurrent variceal hemorrhage (4)
1. Repeated variceal band ligation
2. Beta blockade
3. Portosystemic shunt surgery
4. TIPS
696
Usually the 1st indication of portal hypertension
Hypersplenism with thrombocytopenia
697
Most common cause of ascites
Portal hypertension related to cirrhosis
698
In ascitic patients, at least ____ of fluid in the abdomen before they are aware that there is an increase
1-2 L
699
Hepatic hydrothorax is more common on what side
Right
Rent in the diaphragm with free flow of ascitic fluid into the thoracic cavity
700
Serum ascites-to-albumin gradient (SAAG) that is indicative of portal hypertension
>1.1 g/dL
701
Serum ascites-to-albumin gradient (SAAG) that is indicative of infectious or malignant causes
<1.1 g/dL
702
Absolute PMN level of ascitic fluid that is indicative of infection
> 250/μL
703
Treatment of ascites secondary to cirrhosis (2)
1. Dietary sodium restriction
| 2. Diuretic therapy
704
Dietary sodium restriction in ascites
< 2 g of Na per day
705
Dose of spironolactone and furosemide in ascites secondary to cirrhosis
Spironolactone 100-200 mg/day as a single dose; can be increased to 400-600 mg/d
Furosemide 40-80 mg/day; can be increased to 120-160 g/d
706
Treatment of refractory ascites secondary to cirrhosis (3)
1. Repeated large-volume paracentesis with albumin
2. TIPS procedure
3. Liver transplantation
707
____ of patients survive 2 years after the onset of ascites in cirrhosis
<50%
Poor prognosis
708
Spontaneous infection of the ascitic fluid without an intraabdominal source
Spontaneous bacterial peritonitis
709
Presumed mechanism for development of SBP
Bacterial translocation
710
Most common organism causing SBP
Escherichia coli
Other gut bacteria
Gram-positive bacteria: S. viridans, S. aureus, and Enterococcus sp.
711
Secondary bacterial peritonitis is suspected if ____ organisms are identified in the culture of ascitic fluid
>2
712
Most common cause of secondary bacterial peritonitis
Perforated viscus
713
Clinical presentation of SBP (5)
1. Ascites
2. Fever
3. Altered mental status
4. Elevated WBC
5. Abdominal pain or discomfort
714
T or F. In patients with BEV, prophylaxis for SBP must be given
True
715
Treatment of SBP
3rd generation cephalosporin
716
T or F. Hepatorenal syndrome is a combination of liver and renal pathology.
False. HRS is a form of functional renal failure without renal pathology
717
Clinical feature of hepatorenal syndrome
large amount of ascites in patients who have a stepwise progressive increase in creatinine
718
HRS type with progressive impairment in renal function and a significant reduction in creatinine clearance within 1-2 weeks of presentation
Type 1 HRS
Type 2 HRS – fairly stable
719
Which HRS type has worse outcome?
Type 1 HRS
720
Management of HRS (5)
1. Dopamine or prostaglandin analogues
2. Midodrine – α agonist
3. Octreotide
4. IV albumin
5. Liver transplantation – best therapy
721
Best therapy for HRS
Liver transplantation
722
Alteration in mental status and cognitive function in the presence of liver failure
Hepatic encephalopathy
723
T or F. Development of encephalopathy is a requirement to arrive at a diagnosis of fulminant hepatic failure
True
724
T or F. Brain edema occurs in hepatic encephalopathy
True
725
Sudden forward movement of the wrist when patients extend their arms and bend their wrists back
Asterixis
| “liver flap”
726
Dietary protein used in management of hepatic encephalopathy
vegetable-based protein
727
Mainstay of treatment of hepatic encephalopathy
Lactulose
728
Non-absorbable disaccharide that causes colonic acidification and catharsis in patients with hepatic encephalopathy
Lactulose
729
Dose of rifaximin in hepatic encephalopathy
550 mg BID
730
Vitamin K Dependent clotting factors
II, VII, IX, X
731
Common abnormality in RBC morphology of cirrhotic patients
Macrocytosis
