Gastrointestinal Pathology_1 Flashcards
1
Q
What is dysphagia?
A
difficulty in swallowing
2
Q
what causes dysphagia?
A
diseases that narrow or obstruct the lumen
3
Q
what causes pain and hematemesis?
A
inflammation or ulceration of the esophageal mucosa
4
Q
what is heartburn?
A
retrosternal burning pain
5
Q
what causes heartburn?
A
regurgitation of gastric contents
6
Q
what is the most frequent GI complaint?
A
gas
7
Q
what are esophageal sinuses?
A
blind tubes
8
Q
what are esophageal fistulas?
A
tunnels
9
Q
what is an esophageal perforation?
A
hollow viscous open up into hollow cavity (usually peritoneal cavity)
10
Q
what are the 2 types of esophageal herniations?
A
internal or external
11
Q
what is the most common anemia of GI bleeding?
A
IDA
12
Q
what are the disorders of the esophagus?
A
- dysphagia • 2. pain and hematemesis • 3. heartburn • 4. gas • 5. inflammation and ulcers • 6. sinuses • 7. fistulas • 8. perforation • 9. herniation • 10. bleeding • 11. tumors
13
Q
what are the important structures in the esophagus?
A
- UES= Upper Esophageal Sphincter • 2. LES= Lower Esophageal Sphincter
14
Q
UES is made up of what?
A
skeletal muscle • - cricopharyngeus muscle
15
Q
which esophageal structure is involved in scleroderma?
A
UES
16
Q
where does the LES open up?
A
into the stomach
17
Q
what size is the gastro-esophageal junction?
A
3 cm
18
Q
what is a gastro-esophageal junction >3 cm called?
A
Barrett’s esophagus
19
Q
what is the cell type of the LES transitional zone?
A
columnar
20
Q
what do congenital anomalies of the esophagus do?
A
produce choking on breast feeding
21
Q
what are the congenital anomalies of the esophagus?
A
atresia • fistulas • webs • Schatzki’s rings • Stenosis
22
Q
what is esophageal atresia?
A
noncanalzed segment
23
Q
what are esophageal fistulas?
A
connection/opening between esophagus trachea • - several types
24
Q
how do esophageal webs present?
A
dysphagia to solids
25
what are the clinical features of Plummer-Vinson/Paterson-Kelly syndrome?
post cricoid web • IDA • glossitis • cheilosis in perimenopausal female • risk of postcricoid squamous cell carcinoma
26
What is a type I Tracheoesophageal fistula?
Esophageal agenesis. Very rare
27
What is a type A/2 TEF?
Proximal and distal esophageal bud- a normal esophagus with a missing mid-segment
28
what is a type B/3A TEF?
Proximal esophageal termination on the lower trachea with distal esophageal bud
29
what is a type C/3B TEF?
proximal esophageal atresia (esophagus continuous with the mouth ending in a blind loop superior to the sternal angle) with a distal esophagus arising from the lower trachea or carina
30
what is the most common type of TEF?
Type C/3B
31
what is a type D/3C TEF?
proximal esophageal termination on the lower trachea or carina with distal esophagus arising from the carina
32
what is a type E TEF?
a variant of type D: if the 2 segments of the esophagus communicate, this is sometimes termed an H type fistula due to its resemblance of to the letter H.
33
which fistula is TEF without EA?
Type E/H
34
where do Schatzki's rings present?
LES
35
what do Schatzki's rings cause?
narrowing (stenosis) of esophagus
36
what is the most common cause of esophageal stenosis?
gastro-esophageal reflux
37
is esophageal stenosis more commonly inherited or acquired?
acquired (corrosives, radiation, Scleroderma CREST syndrome)
38
what is the major symptoms associated with esophageal stenosis?
dysphagia
39
what are the esophageal lesions with motor dysfunction?
Achalasia cardia • Hiatal Hernia • True Diverticula • Zenker's (pharyngeal diverticulum) • Epiphrenic diverticulum
40
what age group is affected by achalasia cardia?
adults
41
what is the nature of achalasia cardia?
'failure to relax'
42
what are the clinical features of achalasia cardia?
1. aperistalsis • 2. complete or partial relaxation of LES with swallowing • 3. Increased resting tone of LES
43
what are the complications associated with achalasia cardia?
- aspiration pneumonia • - candidal esophagitis (due to stagnation of food) • - diverticulae • - squamous cell carcinoma (2-5%)
44
achalasia cardia can also be caused by what?
Chaga's disease (Trypanosoma cruzi) • Diabetic autonomic neuropathy
45
what is Hiatal Hernia?
Upward protrusion of part of stomach through the diaphragmatic esophageal foramen
46
what is a true diverticulum?
out-pouching of the esophageal wall (contains all visceral layers)
47
what is a false diverticulum?
out-pouching of mucosa and submucosa only
48
Zenker's (pharyngeal) diverticulum is seen as what?
mass in neck of elderly patient above UES
49
Zenker's diverticulum is due to what?
disordered cricopharyngeal motor dysfunction
50
Zenker's diverticula produce what problems?
food regurgitation and dysphagia
51
what are the features of traction diverticulum?
asymptomatic and located near midpoint of esophagus
52
where is an epiphrenic diverticulum located?
just above the LES
53
epiphrenic diverticulum is caused by what?
dyscoordinated peristalsis and motor dysfuction of LES
54
epiphrenic diverticulum causes what?
regurgitation of food and aspiration pneumonia
55
what is the most common TEF?
C
56
what is the most life threatening TEF?
B: • cough, sputter, suffocate
57
TEF are associated with what?
heart and other GIT anomalies
58
90% of hiatal hernias are which type?
sliding
59
10% of hiatal hernias are which type?
rolling
60
what are the features of sliding hiatal hernia?
shortened esophagus dragging part of the stomach into the thoracic cavity (stomach continuous with the esophagus)
61
what are the features of rolling hiatal hernia?
(para-esophageal hernia) • - part of the stomach (fundus) herniates alongside esophagus into the thorax
62
which hiatal hernia is vulnerable to serious strangulation?
rolling
63
hiatal hernias are prone to what?
ulceration • bleeding • dysphagia
64
what is the site of Mallory-Weiss syndrome?
gastro-esophageal junction (GEJ)
65
what is Mallory-Weiss syndrome caused by?
excessive vomiting in the presence of LES spasm
66
when is Mallory-Weiss syndrome most common?
alcoholics and pregnancy
67
what is the morphology of Mallory-Weiss syndrome?
irregular longitudinal tear in the GEJ involve only the mucosa
68
what is the morphological difference between Boerhaave's syndrome and Mallory-Weiss syndrome?
in Boerhaave's tear penetrates all layers of esophagus
69
what is the clinical presentation of Mallory Weiss tear?
severe hematemesis
70
what is the clinical presentation of Boerhaave's syndrome?
produces mediastinitis or peritonitis
71
what are esophageal varices?
dilated tortuous submucosal veins
72
when are esophageal varices seen?
long-standing cirrhosis with portal HTN
73
how many patients with cirrhosis bleed and die of varices?
50% • MCC of death
74
what are the causes of esophagitis?
1. reflux of gastric contents • 2. Barrett's esophagus
75
what is the most common cause of esophagitis?
reflux esophagitis
76
what part of the esophagus is affected by reflux esophagitis?
distal part
77
what is the clinical presentation of reflux esophagitis?
dysphagia • heartburn • regurgitation • develop Barrett's esophagus in long standing cases
78
Barrett's esophagus is a complication of what?
long-standing gastroesophageal reflux
79
what is Barrett's esophagus?
columnar metaplasia of distal esophagus
80
what is the cancer risk associated with Barrett's?
30 times more risk of adenocarcinoma in the lower esophagus
81
what is the histological presentation of Barrett's esophagus?
gastric type mucosa above the gastroesophageal junction
82
metaplasia in Barrett's results from what?
chronic GERD
83
what is typical barrett's mucosa?
gastric mucosa with intestinalization • - goblet cells in columnar mucosa
84
what is the most common benign tumor of esophagus?
leiomyoma
85
from what does esophageal leiomyoma arise?
smooth muscle cells
86
what is the incidence of squamous cell carcinoma of the esophagus?
common in China • Rare in US (Adenocarcinoma- MC in USA) • M>F • >50yo
87
what are the risk factors for esophageal squamous cell carcinoma?
cigarette smoking • alcohol • nitrosamines in preserved foods • fungus contaminated foods
88
what is the site of squamous cell carcinoma of the esophagus?
50% are in the middle 1/3
89
what is early carcinoma in SCC of esophagus?
up to submucosa
90
what is the prognosis for early carcinoma in SCC of esophagus?
5 yr= 90% even with lymph node involvement
91
to where does esophageal SCC spread?
locally into mediastinal structures and to lymph nodes
92
what are the clinical features of esophageal SCC?
insidious dysphagia • weight loss • hemorrhage • esophago-tracheal fistula
93
what is the overall survival for SCC of esophagus?
5 yr=5%
94
what is the incidence of esophageal adenocarcinoma?
<25% of esophageal cancers world wide • ** up to 50% of esophageal cancer in USA
95
what is the primary risk factor for esophageal adenocarcinoma?
Barrett's esophagus
96
what is site of esophageal adenocarcinoma?
most arise in the distal 1/3rd of the esophagus
97
what is the histology of esophageal adenocarcinoma?
mucin producing tubular (intestinal), or signet cell/ring (gastric/infiltrative) carcinoma, undifferentiated
98
how does esophageal adenocarcinoma present?
dysphagia
99
what is the overall survival of esophageal adenocarcinoma?
15%
100
what is the typical morphology of esophageal SCC?
irregular reddish, ulcerated, exophytic • MC in midesophageal mass seen on mucosal surface
101
what is the typical histological presentation of esophageal SCC?
#NAME?
102
what is the incidence of the malignant esophageal tumors?
squamous= 75% • adenocarcinoma=25%
103
what are the geographic regions most commonly associated with the malignant esophageal tumors?
Squamous= asia • adeno= usa
104
what is the age group MC affected by the malignant esophageal tumors?
squamous >50yo • adeno >40yo
105
what are the sites of the malignant tumors of the esophagus?
squamous= middle 1/3 • adeno= lower 1/3
106
what are the risk factors associated with the malignant tumors of the esophagus?
SCC- smoking, EtOH, foods • adeno- Reflux esophagitis (Barrett's)
107
what is the prognosis for the malignant tumors of the esophagus?
SCC= 5yr= 5% • adeno= 5yr= 15%
108
What are the cells associated with stomach glands and where are they found?
- parietal cells found in the fundus and body • - chief cells are more at fundus and body
109
what do stomach parietal cells secrete?
HCl and IF
110
what do stomach chief cells secrete?
pepsinogen I and II
111
what are the congenital abnormalities of the stomach?
1. diaphragmatic hernia • 2. congenital hypertrophic pyloric stenosis
112
what causes diaphragmatic hernia?
defect in the diaphragm--> away from the hiatal orifice
113
what herniates in a diaphragmatic hernia?
portions of the stomach and small intestines
114
diaphragmatic hernia results in what?
respiratory impairment • pulmonary hypoplasia
115
what is the problem in congenital hypertrophic pyloric stenosis?
hypertrophy of the circular muscle of the pylorus results in regurgitation and vomiting in the neonatal period
116
what is the classic PE finding in congenital hypertrophic pyloric stenosis?
VGP= visible gastric peristalsis • + • palpable mass in the epigastrium
117
what is the inheritance of congenital hypertrophic pyloric stenosis?
males • multifactorial inheritance
118
what is the treatment for congenital hypertrophic pyloric stenosis?
full thickness muscle splitting incision (pyloromyotomy) is curative (Heller's operation)
119
what is acute gastritis?
inflammation of gastric mucosa
120
what cells are associated with acute gastritis?
presence of neutrophils
121
what cells are associated with chronic gastritis?
lymphocytes and plasma cells
122
what is acute gastritis caused by?
ingestion of strong acids or alkalies, • NSAIDs, • cancer chemotherapy, • irradiation, • alcohol, • uremia, • severe stress and shock states
123
what are the proposed mechanisms of acute gastritis?
increased acid production with decreased surface bicarb buffer
124
what is the morphology associated with acute gastritis?
mucosal edema • hyperemia • PML infiltration • erosions (not deeper than muscularis mucosa) • hemorrhages
125
how deep do erosions in acute gastritis penetrate?
not deeper than muscularis mucosa
126
what is the histologic presentation of acute gastritis?
gastric mucosa infiltration by neutrophils
127
what is the gross morphologic presentation of acute gastritis?
diffusely hyperemic gastric mucosa
128
what are the common causes for acute gastritis?
alcoholism • drugs • infections etc
129
what is chronic gastritis?
chronic mucosal inflammation leading to mucosal atrophy, intestinal metaplasia, and dysplasia
130
what is the MCC of chronic gastritis?
chronic infection by H. pylori
131
what is the mechanism of chronic gastritis caused by H. pylori?
elaboration of urease produces ammonia that buffers gastric acid, protecting organism from acid
132
what are the other diseases (besides chronic gastritis) associated with H. pylori infection?
peptic ulcer disease • gastric carcinoma • gastric lymphoma
133
what causes 10% of chronic gastritis?
autoimmunity: • Ab to parietal cells cause parietal cell destruction (HCl +IF)
134
what is the histological presentation of H. pylori that causes chronic gastritis?
#NAME?
135
how is H pylori in chronic gastritis visualized?
stain with methylene blue
136
what is the problem associated with autoimmune gastritis?
pernicious anemia
137
chronic atrophic gastritis is associated with antibodies against what?
IF • parietal cell
138
what is a gastric ulcer?
a breach in mucosa and extends through muscularis mucosae into submucosa or deeper
139
what is acute erosive gastritis?
erosions above the muscularis mucosa
140
acute gastric ulcers are caused by what?
severe stress • shock/extensive burns • severe head injury • patients in ICU
141
what is the name for acute erosive gastritis caused by severe stress?
stress uclers
142
what is the name for acute erosive gastritis caused by shock, extensive burns?
Curling's ulcers
143
what is the name for acute erosive gastritis caused by severe head injuries?
Cushing's ulcers
144
what is the cause of acute erosive gastritis in patients in ICU?
use of NSAIDs
145
what is the morphology of acute gastric ulcers?
multiple, small (<1cm ulcers) normal adjacent mucosa
146
what is the clinical presentation of acute gastric ulcers?
upper GIT hemorrhage
147
what is the Tx for acute gastric ulcers?
treat underlying cause
148
what do stress ulcers look like?
small, shallow gastric ulcerations
149
chronic peptic ulcers are characterized by what?
solitary, chronic ulcers
150
what is the ratio of duodenal to gastric chronic peptic ulcers?
4:01
151
what is the more common chronic peptic ulcer?
duodenal
152
what is the morphology of chronic peptic ulcer?
sharply punched out mucosal defect with sharp borders and clean ulcer base • - surrounding mucosa shows chronic gastritis & radial convergence of rugal folds towards the ulcer niche (unlike malignant ulcer)
153
how do chronic peptic ulcers present clinically?
epigastric pain 1-3h after meals and worse at night; nausea; vomiting; belching; occult blood in the stool
154
what are the complications of chronic peptic ulcers?
perforation • hemorrhage • obstruction • malignant transformation
155
perforation accounts for how many ulcer deaths?
03-Feb
156
hemorrhage accounts for how many ulcer death?
25%
157
what does obstruction caused by peptic ulcer cause?
severe crampy abdominal pain
158
how common is malignant transformation in peptic ulcer?
extremely rare
159
what are the normal damaging forces in the stomach?
gastric acidity • peptic enzymes
160
what are the normal defensive forces in the stomach?
1. surface mucus secretion • 2. bicarbonate secretion into mucus • 3. mucosal blood flow • 4. apical surface membrane transport • 5. epithelial regenerative capacity • 6. elaboration of prostaglandins
161
what are the forces that lead to increased damage in the stomach and can produce ulcer?
H pylori infection • NSAID • ASA • Cigs • EtOH • gastric hyperacidity • too rapid gastric emptying • psych stress
162
what are the impaired defensive forces in the stomach that can lead to peptic ulcer?
1. decreased mucus secretion • 2. decreased PG synth • 3. delayed gastric emptying
163
what are the microscopic features of gastric ulcer?
sharply demarcated • normal gastric mucosa falling away into deep ulcer whose base contrains inflamed necrotic debris
164
hypertrophic gastropathy is characterized by what?
giant enlargement of the gastric rugal folds
165
hypertrophic gastropathy is caused by what?
hyperplasia of epithelial cells (not due to inflammation)
166
what is the malignant risk associated with hypertrophic gastropathy?
increased risk of cancer
167
what are the 3 variants of hypertrophic gastropathy?
- Menetrier's disease • - Hypersecretory Gastropathy • - Zollinger-Ellison syndrome
168
what is another name for Menetrier's disease?
protein losing gastropathy
169
what are the features of Menetier's disease?
- hyperplasia of surface mucus cells • - glandular atrophy • - excessive loss of proteins in gastric secretion
170
what are the features of hypersecretory gastropathy?
- hyperplasia of parietal and chief cells • - secondary to excessive gastrin stimulaton
171
what is the cause of Zollinger-Ellison syndrome?
gastrinoma of the pancreas secreting gastrin--> elevated serum gastrin levels
172
what are the features of Zollinger-Ellison syndrome?
- multiple peptic ulcerations in stomach, duodenum, jejunum • - hypertrophic rugal folds and parietal cell hyperplasia--> excessive gastric acid production
173
what are the benign tumors of the stomach?
gastric polyps • adenomatous polyps
174
how many gastric polyps are neoplastic?
90% non-neoplastic= • hyperplastic or inflammatory
175
do non-neoplastic gastric polyps have malignant potential?
no
176
what is the tx for gastric polyps?
biopsy
177
what are adenomatous polyps in the stomach?
true neoplasms with proliferative dysplastic epithelium
178
do adenomatous polyps of the stomach have malignant potential?
yes, common in old age
179
adenomatous polyps of the stomach are MC associated with what?
chronic gastritis or familial polyposis syndromes
180
what are the malignant tumors of the stomach?
1. Gastric carcinoma • 2. Gastrointestinal Stromal Tumor • 3. carcinoid (neuroendocrine) tumors • 4. gastric lymphoma
181
what is the incidence of gastric carcinoma?
4 fold decline in incidence over the last 70 years for unknown reasons
182
what are the dietary risk factors for gastric carcinoma?
nitrites (from food preservatives), smoked and salted foods, deficiency of fresh fruits and vegetables
183
what are the host factor risk factors for gastric carcinoma?
chronic gastritis (autoimmune & H. pylori), adenomatous polyps, partial gastrectomy pt
184
what are the genetic risk factors for gastric carcinoma?
blood group A • close relatives of stomach cancer patients • certain racial groups (Japanese)
185
what are the classifications of Gastric Carcinoma?
1. early gastric carcinoma • 2. advanced gastric carcinoma
186
what is early gastric carcinoma?
confined to the mucosa & submucosa, despite lymph node spread
187
what is the prognosis for early gastric carcinoma?
associated with very good prognosis >90% 5yr
188
what is advanced gastric carcinoma?
has extended beyond the submucosa & spread is by local invasion, lymphatics, blood (to liver and lungs)
189
what is Krukenberg tumor?
bilateral ovarian metastases (stomach, breast, pancreas, even gallbladder)
190
what is Virchow node?
left supraclavicular node with mets
191
what is the sister Mary Joseph nodule?
metastasize to the periumbilical region (subQ malignant nodule)
192
what are the histologic types of gastric carcinoma?
intestinal type • gastric type
193
what are the features of intestinal type gastric carcinoma?
glandular, expansile growth pattern
194
what are the features of gastric type gastric carcinoma?
diffuse 'signet ring' infiltrating pattern
195
what is the most important prognostic indicator in gastric carcinoma?
pathologic stage
196
from what do GISTs arise?
interstitial cells of Cajal
197
what are the markers of GISTs?
c-KIT (CD117) & CD34 positive
198
what are carcinoid (neuroendocrine) tumors of the stomach made of?
made of ECL cell tumors
199
carcinoid neuroendocrine tumors of the stomach are associated with what diseases?
MEN1 • Zollinger-Ellison Syndrome
200
what is the most common site for extranodal lymphoma?
gastric lymphoma
201
majority of gastric lymphoma are associated with what?
80% associated with H pylori chronic gastritis
202
when are most gastric adenocarcinomas in the US found?
at a late stage when the neoplasm has invaded and/or metastasized
203
what is a cautious approach for early detection of gastric carcinoma?
all gastric ulcers and all gastric masses must be biopsied
204
what is the level of malignancy of duodenal peptic ulcers?
virtually all are benign
205
what is linitis plastica?
diffuse infiltrative gastric adenocarcinoma
206
what are the features of linitis plastica?
- stomach looks like shrunken leather bottle • - markedly thickened gastric wall • - very poor prognosis
207
which type of gastric carcinoma typically produces krukenberg tumor?
gastric type
208
what structures make up the small intestine?
duodenum • jejunum • ileum
209
what is the purpose of the villi and microvilli in the small intestine?
increase surface area of the mucosa
210
what are the crypts of Lieberkuhn
pits between the bases of the villi in small intestine
211
what is the normal villus:crypt height ratio?
4:01
212
where are the digestive enzymes in small intestines located?
in the membranes of microvilli
213
how do bile ducts connect to the small intestine?
common bile duct and pancreatic duct empty into the 2nd part of the duodenum
214
what types of glands are found in the duodenum?
Brunner's glands
215
what are the lymphoid structures in the ileum?
Peyer's patches
216
what are the structures of the large intestine?
1. cecum & its appendix • 2. colon • - ascending • - transverse • - descending • - sigmoid • 3. rectum • 4. anal canal
217
are there villi and microvilli in the large intestine?
large intestine lacks villi and microvilli
218
does the large intestine have goblet cells?
has numerous goblet cells in the mucosa
219
what is the function of the large intestine?
absorption of fluids, electrolytes and secretion of mucus
220
what is the arterial supply of the intestines up to the hepatic flexure of the colon?
SMA
221
what is the arterial supply to the intestine from the hepatic flexure to the rectum?
IMA
222
what are the arterial interconnections in that supply the intestines called?
mesenteric arcades
223
what is the artery that supplies the upper rectum?
superior hemorrhoidal artery from IMA
224
what is the artery that supplies the lower rectum?
hemorrhoidal artery from internal iliac or internal pudendal artery
225
what is the distribution of venous drainage of the intestines?
same as the arterial supply
226
which intestinal vessels connect to form portal and systemic connections?
anastomotic capillary beds between superior and inferior hemorrhoidal veins
227
are the ascending and descending colon intra- or retroperitoneal?
retroperitoneal
228
where does the accessory blood supply and lymphatic drainage of the ascending and descending colon come from?
posterior abdominal wall
229
do lymphatics have arcades?
no • run as parallel vessels without arcades
230
what is the lymphoid tissue in the intestines?
MALT • mucosa associated lymphoid tissue
231
what is the grossly visible lymphoid structure associated with the ileum?
Peyer's patches
232
what is the function of immune M cells in the intestines?
M (membranous cells) transport Ag to APC in SI and LI
233
what is the direction of small intestinal peristalsis?
anterograde and retrograde
234
what is peristalsis in the intestines mediated by?
intrinsic (myenteric plexus) and extrinsic (autonomic innervation) neural control
235
what are the parts of the myenteric plexus?
meissner plexus (in submucosa) • auerbach plexs (muscle wall layers)
236
what differentiates large from small intestine?
large intestine lacks villi and has numerous goblet cells
237
what are the general symptoms associated with intestinal pathology?
1. anorexia • 2. nausea • 3. vomiting • 4. flatulence • 5. bloating • 6. abdominal discomfort • 7. weight loss • 8. malaise
238
what are the esophagus-specific symptoms of GI pathology?
dysphagia • odynophagia • heartburn • regurgitation • retrosternal pain
239
what are the gastric-specific symptoms of GI pathology?
early satiety • hematemesis • upper abdominal pain/discomfort
240
what are the small intestine specific symptoms of GI pathology?
diarrhea • steatorrhea • anemia • abdominal colic
241
what are the large intestine specific symptoms of GI pathology?
diarrhea • constipation • blood and mucus per rectum • tenesmus • proctalgia • anemia
242
what are the congenital anomalies of the intestines?
- atresia and stenosis • - meckel diverticulum • - Hirschsprung disease
243
what is atresia?
complete obstruction
244
what is the most common site of intestinal atresia?
duodenum
245
what is the common cause of neonatal intestinal obstruction?
duodenal atresia
246
what is the frequency of jejunum and ileum atresia?
jejunum and ileum are equally involved, less so than the duodenum, but more so than the colon
247
how often does atresia of the colon happen?
never
248
what is stenosis?
incomplete obstruction
249
what is more common, intestinal atresia or stenosis?
atresia
250
what is imperforate anus?
failure of cloacal diaphragm to rupture--> • neonatal intestinal obstruction
251
what type of diverticulum is Meckel's diverticulum?
true diverticulum
252
what is the 2% rule of Meckel's diverticulum?
2 feet from ileocecal valve, seen i 2% of people, 2" in size
253
what are the symptoms of Meckel's diverticulum?
asymptomatic
254
what is in Meckel's diverticulum?
may contain gastric or pancreatic tissues &(peptic ulcers, diverticulitis, intestinal obstruction, intussusception)
255
what is the cause of Meckel's diverticulum?
persistent segment of the vitelline duct (h connects the yolk sac + gut lumen)
256
what is another name for Hirschsprung's disease?
aganglionic megacolon
257
what causes Hirchsprung's disease?
arrested migration of nerve elemets into distal part of gut
258
what is Hirschsprung's disease?
absence of ganglion cells in the large bowel (Aurbach's and Meissner's plexus)
259
50% of familial and 15% of sporadic cases of Hirschsprung's disease are due to what?
mutations in the RET gene
260
what does the RET gene do?
promote survival and growth of neurite and direction to migrating neural crest cells
261
Hirschsprung's disease is characterized by what?
aganglionic (aperistaltic) segment--> narrow unaffected proximal colon--> dilation and hypertrophy (megacolon)
262
there is an increased risk of Hirschsprung's disease with what condition?
down syndrome
263
what is the incidence of Hirschsprung's disease?
1:8000 live births • M:F=4:1
264
how does Hirschsprung's disease present?
meconium ileus • abdominal distention • constipation • diarrhea (enterocolitis) • perforation (rare)
265
what is involved in the diagnosis of hirschsprung's disease?
histological demonstration of absence of ganglion cells in intestinal submucosa
266
how is a biopsy suspicious for Hirschsprung's treated for lab dx?
stained for acetyl cholinesterase
267
what are the conditions important in the differential diagnosis of Hirschsprung's disease?
any acquired megacolon: • 1. Chagas disease • 2. Obstruction (neoplastic) or inflammatory stricture of the bowel • 3. toxic megacolon- ulcerative colitis or Crohn disease • 4. functional causes
268
what is diarrhea?
frequent passage of loose watery stools
269
what is secretory diarrhea?
passage of >500ml/day of watery stools, isotonic with plasma (intestinal secretion)
270
what is osmotic diarrhea?
>500mL/d stools, the osmolality of which exceeds that of plasma by >50 mOsm
271
what is exudative diarrhea?
frequent passage of loose, purulent, bloody stools
272
what is dysentery?
painful bloody diarrhea (tenesmus)
273
what does malabsorption look like?
bulky stools with excess fat (floats on water) and increased osmolality
274
what is the volvume/day of secretory diarrhea?
>500mL
275
what is the volume/day of osmotic diarrhea?
>500mL
276
what is the volume of stool in malabsorption?
large volume
277
what is the osmolarity of stool with respect to plasma in secretory diarrhea?
isotonic
278
what is the osmolarity of stool with respect to plasma in osmotic diarrhea?
>50mOsm hypertonic
279
what is the osmolarity of stool with respect to plasma in malabsorption?
hypertonic
280
does secretory diarrhea persist on fasting/
yes
281
does osmotic diarrhea persist on fasting?
no
282
does exudative diarrhea persist on fasting?
yes
283
does malabsorption diarrhea persist on fasting?
no
284
is there steatorrhea in secretory diarrhea?
no
285
is there steatorrhea in osmotic diarrhea?
no
286
is there steatorrhea in exudative diarrhea?
no
287
is there steatorrhea in malabsorption diarrhea?
yes
288
is there blood/pus in secretory diarrhea?
no
289
is there blood/pus in osmotic diarrhea?
no
290
is there blood/pus in exudative diarrhea?
yes
291
is there blood/pus in malabsorption diarrhea?
no
292
what are the types of infective enterocolitis?
1. viral • 2. bacterial • 3. bacterial overgrowth syndrome • 4. parasitic EC • 5. necrotizing EC • 6. collagen & lymphocytic EC
293
what is infective enterocolitis?
acute, self limited infectious diarrhea
294
infective enterocolitis is a major cause of morbidity among which population?
children
295
what is the most common cause of infective enterocolitis?
enteric viruses
296
viral enterocolitis is characterized by what?
food and water infections that cause damage of small intestinal epithelium with shortening of villi • - diarrhea for 1-7 days
297
what are the most common causes of viral enterocolitis?
1. Rotavirus (Group A) • 2. Norwalk Virus • 3. Adenovirus
298
who is affected by Rotavirus Group A infections?
outbreaks in children 6-24 months
299
what happens in rotavirus group A EC?
selectively infects and destroys mature enterocytes in the small intestine, without infecting crypt cells
300
what are the features of Norwalk virus EC?
food borne nonbacterial outbreaks in school children and adults
301
adenovirus EC outbreaks affect which populations?
infants
302
what do the morphologic changes in bacterial EC depend on?
the causative agent
303
what are the pathogenic mechanisms underlying bacterial EC?
1. ingestion of preformed toxins • 2. infection by toxigenic orgnisms
304
Bacterial EC can be caused by ingestion of preformed toxins present in contaminated food by what organisms?
Staph. aureus • Clost. perfringens • Virbrios
305
what are the 2 ways that bacterial EC caused by infection by toxigenic organisms proliferate?
1. proliferate within gut lumen and elaborate an enterotoxin • 2. proliferate, invade, and destroy mucosal epithelial cells
306
which organisms that cause bacterial EC proliferate within the gut lumen and elaborate an enterotoxin?
enteroinvasive organisms: • - E coli • - Shigella • - Salmonella
307
what are the 2 types of enterotoxins associated with bacterial EC?
secretagogues (cholera toxin) • cytotoxins (Shiga toxin)
308
what are the clinical features of bacterial EC caused by ingestion of preformed toxins?
- develop within a matter of hours • - explosive diarrhea • - actue abdominal distress • - passes in a day or so
309
what are the clinical features of bacterial EC caused by infection with enteric pathogen?
- incubation period of several hours to days • - followed by diarrhea and dehydration
310
what are the complications associated with bacterial EC?
- massive fluid loss or destruction of intestinal mucosal barrier • - dehydration, sepsis, perforation
311
what are the major sources Salmonella in the USA?
Feces contaminated beef and chicken
312
what is the more common organism that causes bacterial EC from chicken?
Campylobacter jejuni • - more common than Shigella and Salmonella
313
how does cholera toxin cause secretory diarrhea?
1. permanently activate GTP--> persistent activation of adenylate cyclase--> high levels of intracellular cAMP--> stimulates secretion of chloride and bicarb • 2. chloride and sodium reabsorption is inhibited
314
what is another name for pseudomembranous colitis?
antibiotic associated colitis (EC)
315
what type of colitis is pseudo-membranous colitis?
acute colitis
316
what is pseudo-membranous colitis caused by?
enterotoxins of Clostridium dificile
317
what is the role of the enterotoxins of Colstridium dificile in pseudomembranous colitis?
due to toxins A and B--> cytokine production--> cell apoptosis
318
antibiotic associated colitis is characterized by what?
the formation of an adherent necrotic membrane (pseudomembrane) overlying extensive mucosal inflammation
319
what makes up the pseudomembrane associated with pseudomembranous colitis?
mucus, fibrin, and inflammatory debris
320
similarly to pseudomembranous colitis, fibrinopurulent necrotic pseudomembrane forms in what?
enteroinvasive infections • ischemic EC
321
what are the clinical features of pseudomembranous colitis?
- presents as acute diarrhea while on antibiotic therapy • - toxin detectable in stools • - responds to appropriate antibiotics
322
what is the cause of bacterial overgrowth syndrome?
surgical procedures- decreasing the time for exposure of ingested bacteria to gastric acid • - bacterial overgrowth in the small intestine
323
how does bacterial overgrowth syndrome present clinically?
chronic diarrhea • abdominal pain • malabsorption • weight loss
324
what is involved in the diagnosis of bacterial overgrowth syndrome?
- breath tests for volatile bacterial byproducts • - clinical history • - demonstration of bacteria in the proximal small intestine by direct culture
325
what are the nematodes that cause parasitic EC?
1. ascaris lumbricoides • 2. strongyloides • 3. hookworm • - necator duodenale • - ancylostoma duodenale • 4. enterobius vermicularis (pinworm) • 5. trichuris trichiuria (whipworm)
326
what is the most common nematode cause of parasitic EC?
ascaris lumbricoides
327
what are the features of parasitic EC caused by ascaris lumbricoides?
- obstruct the intestine or biliary tree • - pneumonitis • - hepatic abscess
328
how is ascaris lumbricoides diagnosed?
detection of eggs in the feces
329
what are the features of parasitic EC caused by strongyloides?
- pulmonary infiltrates with eosinophilia • - autoinfection in immnosuppressed
330
what are the features of parasitic EC caused by the hookworms necator duodenale or ancylostoma duodenale?
- intestinal mucosa erosions, focal hemorrhage • - long term infection lead to IDA
331
what are the features of parasitic EC caused by pinworm enterobius vermicularis?
perianal pruritus
332
what causes perianal pruritus in parasitic EC caused by enterobius vermicularis?
worms migrate to the anal orifice and deposit eggs
333
how is enterobius vermicularis diagnosed?
perianal skin tape
334
what are the features of parasitic EC caused by trichuris trichiura?
- Heavy infections- cause bloody diarrhea and rectal prolapse • - in young children
335
what are the features of parasitic EC caused by cestodes?
- never invade beyond the intestinal mucosa • - no eosinophilia
336
what are the cestodes that cause parasitic EC?
Diphyllobothrium latum (fish tapeworm) • Taenia solium (pork tapeworm) • Hymenolepsis nana (dwarf tapeworm)
337
what are the protozal infections that cause parasitic EC?
1. Amebiasis (Entamoeba histolytica) • 2. Giardiasis
338
what is the site of infection in parasitic EC caused by Amebiasis vs. Giardiasis?
Amebiasis= LI (cecum and ascending colon) • Giardiasis= SI (duodenum)
339
what is the difference in the stool caused by parasitic EC from amebiasis vs giardiasis?
Amebiasis= dysentery • Giardiasis= diarrhea
340
what type of ulcers are present in parasitic EC caused by amebiasis vs giardiasis?
amebiasis= flask shaped ulcer • giardiasis= no ulcers
341
what is the difference between trophozoites in amebiasis vs giardiasis?
amebiasis= 1 nucleus • giardiasis= 2 nuclei
342
what is the difference between the flagella of the organisms that cause amebiasis vs giardiasis?
amebiasis= no flagella • giardiasis= flagellated
343
what is the difference between the treatment for amebiasis vs giardiasis?
rx is same for both
344
what is the most common acquired gastrointestinal emergency?
necrotizing enterocolitis
345
which babies are at highest risk for necrotizing enterocolitis?
premature • low birth weight
346
what causes necrotizing enterocolitis?
immaturity of the gut immune system
347
necrotizing enterocolitis is characterized by what?
necrotizing inflammation of the small and large intestine
348
what happens in necrotizing enterocolitis?
initiation of oral feeding--> release of cytokines (PAF)--> inflammatory response • --> gut colonization with bacteria • --> mucosal injury
