Chapter 17- The GI Tract Flashcards
1
Q
What congenital anomalies are common in the GI tract?
A
Atresia
Fistula
Stenosis
Congenital duplication cysts
Diaphragmatic hernia
Omphalocele
Gastroschisis
Ectopia
Meckel diverticulum
Congenital hypertrophic pyloric stenosis
Hirschsprung disease
2
Q
What is the most common form of intestinal atresia?
A
Imperforate anus
3
Q
What is esophageal atresia associated with?
A
A fistula connecting the upper or lower esophageal pouches to a bronchus or the trachea
4
Q
Esophageal atresia causes what form of obstruction?
A
Mechanical
5
Q
What is the most common site of intestinal fistula?
A
Esophagus-trachea
6
Q
Stenosis is an incomplete form of what?
A
Atresia
7
Q
What causes stenosis?
A
Fibrous thickening of the wall
8
Q
What areas of the GI tract does stenosis commonly affect?
A
Esophagus
Small intestine
9
Q
What are congenital duplication cysts?
A
Masses with redundant smooth muscle layers
10
Q
What is a diaphragmatic hernia?
A
An incomplete diaphragm allows the abdominal viscera to herniate into the thoracic cavity
11
Q
What is the difference between an omphalocele and gastroschisis?
A
Omphalocele- abdominal musculature is incomplete, viscera herniates into the ventral membranous sac
Gastroschisis- involves all the abdominal wall layers, not just the musculature, not contained
12
Q
What is the most common form of intestinal ectopia?
A
Gastric mucosa in the upper third of the esophagus (acid production)
13
Q
What are the features of Meckel diverticulum?
A
Blind outpouching of the GI tract
Includes all three layers of the bowel wall
Occurs in the ileum (2ft of ileocecal valve)
Tip shows ectopia tissue
Pouch is antimesenteric
14
Q
How does Meckel diverticulum occur?
A
Failed involuntary of the vitelline duct
15
Q
How does Meckel diverticulum differ from acquired?
A
Acquired only lacks the muscularis layer (or show diminished muscularis propria)
16
Q
What is congenital hypertrophic pyloric stenosis?
A
Hyperplasia of the pyloric muscularis propria, obstructs gastric outflow
17
Q
What are the characteristics of congenital hypertrophic pyloric stenosis?
A
Onset at 3-6th week
Regurgitation, nonbilious vomiting after feeding
Firm ovoid mass
Left to right hyperperistalsis during feeding
18
Q
What increases the risk of congenital hypertrophic pyloric stenosis?
A
Male
Monozygotic twins
Turner syndrome and trisomy 18
Exposure to erythromycin and azithromycin in first 2 weeks of life
19
Q
What is Hirschsprung disease?
A
Aganglionic megacolon (loss of bowel innervation)
20
Q
How does Hirschsprung disease occur?
A
Neural crest cell migration from the caecum to the rectum is arrested
Distal segment lacks Meissner submucosal and Auerbach mesenteric plexus
21
Q
What are the characteristics of Hirschsprung disease?
A
Impaired peristalsis
Functional obstruction
Dilation proximal to affected segment
Mucosal inflammation or shallow ulcers
22
Q
What disorders can cause esophageal obstruction?
A
Spasms
Diverticuli
Mucosal webs
Esophageal/Schatzki rings
Achalasia
23
Q
What type of obstruction is caused by esophageal spasms?
A
Functional
24
Q
What are the different types of esophageal diverticuli and where are they found?
A
Zenker- above upper esophageal sphincter
Traction- midpoint
Epiphrenic- above lower esophageal sphincter
25
How many walls do esophageal diverticuli involve?
One or more
26
What are mucosal webs?
Ledge-like protrusions of mucosa
27
What is Plummer-Vinson syndrome?
Constellation of mucosal webs, IDA, glossitis and Cheilosis
28
What is another name for Plummer-Vinson syndrome?
Paterson-Brown-Kelly syndrome
29
How do esophageal rings differ from mucosal webs?
Rings are thicker and circumferential
30
What are the two types of esophageal rings and what are their characteristics?
A- squamous epithelium above the gastroesophageal junction
B- gastric cardiac mucosa at the squamocolumnar junction
31
What is achalasia?
Triad of incomplete LES relaxation, increased LES tone and esophageal aperistalsis
32
What causes primary achalasia?
Failure of distal esophageal neurons to induce LES relaxation or degenerative changes in neuron innervation
33
What can cause secondary achalasia?
Chaga’s
Disorders of vagaries dorsal motor nuclei
Diabetic autonomic neuropathy
Infiltrative disorders
34
What are the chief symptoms of esophagitis?
Pain
Dysphagia
35
What can cause esophagitis?
Lacerations (Mallory Weiss tears)
Chemicals
Infections- HSV, CMV, candida
Reflux
36
How do the ulcers in esophagitis caused by HSV and CMV differ?
HSV- punched out
CMV- shallower
37
What is the most common cause of esophagitis?
Reflux
38
What causes reflux?
Decreased LES tone
Increased abdominal pressure
Hiatal hernia
39
What are the characteristics of esophagitis caused by reflux?
Ulceration, hematemesis, melena, stricture, Barrett esophagus
Nasal zone hyperplasia
Elongation of lamina propria papillae
40
What are the characteristics of eosinophilic esophagitis?
Dysphagia and feeding intolerance (GERD-like symptoms)
Large number of superficial intraepithelial eosinophils
Mostly atopic
41
What are esophageal varices?
Congested subepithelial and submucosal venous plexi
Tortuous, dilated veins within the submucosal of the distal esophagus and proximal stomach
42
What types of patients are esophageal varicies seen in?
Cirrhotic patients (hypertension)
Alcoholic liver disease
Schistomiasis infections
43
Barrett esophagus is a complication of what?
Chronic GERD
44
What is Barrett esophagus?
Intestinal metaplasia within the esophageal mucosa (glandular tissue replaces squamous)
45
What is Barrett esophagus a precursor lesion to?
Esophageal adenocarcinoma
46
What is required for the diagnosis of Barrett esophagus?
Endoscopic evidence of metaplastic columnar mucosa above the gastroesophageal junction
47
What is the gross morphology of Barrett esophagus?
Tongues of velvety red mucosa extending upwards from the gastroesophageal junction
48
The majority of esophageal tumours are what kinds?
Adenocarcinoma
Squamous cell carcinoma
49
What is the most common form of benign esophageal tumours?
Leiomyomas
50
Adenocarcinoma in the esophagus normally evolves from what?
Barrett esophagus
51
Where is SCC often found in the esophagus?
Middle third
52
What is the pathology of acute gastritis?
Neutrophils present
Mechanisms that protect the mucosa are overwhelmed/defective
53
What are causative agents of acute gastritis?
NSAIDS
Alcohol
Bile
Stress-induced injury
54
What are the types of ulcers associated with acute gastritis and when do they occur?
1. Stress- shock, sepsis, severe trauma
2. Curling- in the proximal duodenum after severe burns or trauma
3. Cushing- in the esophagus, duodenum and stomach of patients with intracranial disease
55
How do NSAIDS cause ulcers?
Inhibit COX-dependent synthesis of PGE2 and I2 (stimulate defence mechs)
56
What is the morphology of stress-related ulcers?
Small, diffuse
Stained brown/black
57
How does intracranial injury cause ulcers?
Stimulates vagal nuclei (hypersecretion of gastric acid)
58
What is the most common cause of chronic gastritis?
H. pylori
59
Where does H. pylori most often cause chronic gastritis?
Antrum (increased acid production)
60
What is the gross morphology associated with gastritis caused by H. pylori?
Erythmatous, coarse, nodular mucosa
61
Chronic gastritis due to H. pylori can progress to what?
Multifocal atrophic gastritis
Intestinal metaplasia
62
Chronic gastritis not caused by H. pylori is the result of?
Autoimmune disorder or peptic ulcer disease
63
Autoimmune gastritis normally spares what area of the stomach?
The antrum
64
What is autoimmune gastritis associated with?
Hypergastrinemia
65
What is the gross morphology of autoimmune gastritis?
Rugal folds lost
Diffuse mucosal damage in body and fundus
Inflammatory infiltrate
66
What is PUD?
Chronic mucosal ulceration
67
What is the morphology of PUD?
Solitary ulcers with punched out defects and a clean base
68
What is the cause and morphology of hypertrophic gastropathies?
Epithelial hyperplasia linked to excessive GF production
Giant enlargement of rugal folds
69
What are two forms of hypertrophic gastropathies?
1. Menetrier disease
| 2. Zollinger-Ellison syndrome
70
What is the pathology of Menetrier disease?
Folveolar cell hyperplasia in body and fundus
Protein losing enteropathy (hypoproteinemia)
71
What is the pathology of Zollinger-Ellison syndrome?
Gastronomes in the small bowel or pancreas increase gastric release
Increased number of gastric parietal cells and HCl production
Ulcers and/or diarrhea
72
What are the different types of benign gastric polyps and what are their characteristics?
Inflammatory and hyperplastic- less than 1cm, multiple lesions, can have surface ulceration
Fundic gland- single or multiple smooth, well circumscribed lesions
Gastric adenoma- usually solitary and greater than 2cm
73
What percentage of gastric adenomas harbour carcinoma?
30%
74
What is the most common form of gastric malignancies?
Adenocarcinoma
75
What is important for the oncogenesis of adenocarcinoma?
Loss of intracellular adhesion (E-cad)
76
Adenocarcinoma affects what areas of the stomach most?
Antrum > lesser curve > greater curve
77
Gastric adenocarcinoma is associated with what?
H. pylori
N-nitro compounds
Benzo-alpha-pyrene
78
What are the two forms of gastric adenocarcinoma and their characteristics?
1. Intestinal- bulky, exophytic masses with glandular structures and flat dysplasia
2. Diffuse- signet ring cells, no glands with flat desmoplastic response (thickened wall/linitus plastic)
79
What does the prognosis of gastric adenocarcinoma depend on?
Depth of invasion
Node involvement
80
Extranodal lymphoma is common where?
The stomach
81
What cells do carcinoid tumours arise from?
Endocrine
82
What is the morphology of carcinoid tumours in the stomach?
Yellow-tan intramural or submucosal masses forming polyploid lesions
Scant cytoplasm, stippled nuclei, positive for chromogranin A and synaptophysin
83
What are two types of gastric carcinoid tumours and their characteristics?
Zollinger-Ellison syndrome- gastrin carcinoids
Carcinoid syndrome- cutaneous flushing, bronchospasm, bowel motility, RS cardiac valance thickening
84
What is the most important prognostic factor of carcinoid tumours?
Primary site
85
What is the prognosis for carcinoid tumours in the fore-, mid- and hindguts?
Fore- resection cures
Mid- multiple and aggressive
Hind- benign, found incidentally
86
Gastrointestinal stromal tumours (GISTs) arise from what cells?
Interstitial cells of Cajal (peristaltic cells)
87
What is the morphology of GIST?
Solitary, well circumscribed, fleshy masses
Up to 30cm
Epitheloid or spindle cell shaped
88
75% of GIST patients have what mutation?
C-KIT
89
What is the Carney Triad?
1. Nonhereditary syndrome with GIST
2. Paraganglioma
3. Pulmonary chondromas
90
What part of the intestine is most commonly involved in obstruction?
Small intestine
91
What are the most common causes of intestinal obstruction and what are their characteristics?
Hernia- defect in peritoneal wall permits peritoneal sac protrusion
Adhesions- healing from inflammation causes fibrous bridging between viscera
Volvulus- complete twisting of a bowel loop about its mesenteric base
Intrassusception- segment telescopes into the immediate distal segment of intestine
92
What areas of the intestine are most vulnerable to hypoperfusion?
Watershed zones
93
What cells are most susceptible to damage due to hypoperfusion and why?
Epithelial cells
Tips of villi
Located in lumen (furthest from blood supply in mesentary)
94
What are the phases of ischemic bowel injury?
1. Initial hypoxic injury
| 2. Reperfusion injury
95
Differentiate intestinal mural and trans mural infarctions.
Mural- complete mucosal necrosis, no serositis
Transmural- involves entire wall thickness, segments are hemorrhagic, serositis, coagulation necrosis with perforation, wall fibrosis, sometimes stricture formation
96
What is angiodysplasia?
Tortuous, ectatic dilations or mucosal and submucosal vessels
97
What are the most common locations of angiodysplasia?
Caecum
Right colon
98
What is steatorrhea and what is it associated with?
Excessive fecal fat
Malabsorption
99
What is the pathogenesis of malabsorption?
Disturbances in intraluminal digestion, terminal digestion, transepithelial support and lymph transport
100
What is celiac disease?
Immune mediated, diarrheal disorder triggered by the ingestion of gluten
101
What protein in gluten causes celiac disease? How does it exert its effects?
Alpha gliadin
Induces epithelial IL-15 expression with CD8 activation and binds APCs to activate CD4 cells
Cytokine mediated epithelial damage
102
What is the morphology of celiac disease?
Diffuse, flattened, atrophic villi and elongated crypts
103
Where is severity greatest in celiac disease?
Proximal intestine
104
10% of celiac patients have what skin disorder?
Dermatitis herpetiforms
105
Celiac disease increases the risk for what?
T-cell lymphoma
Small intestine adenocarcinoma
106
Where is severity greatest in patients with tropical sprue?
Distal small bowel
107
What are the characteristics of autoimmune enteropathy?
X-linked disorder of children
Persistent diarrhea
108
How does lactase deficiency cause diarrhea and malabsorption?
Unabsorbed lactose exerts osmotic pull
109
What are the characteristics of abetalipoproteinemia?
Lipids are unable to leave absorptive cells
Failure to thrive, diarrhea, steatorrhea, absence of apolipoprotein B lipids
Acanthocytes, lipid vacuolation
110
What is the mutation is abetalipoproteinemia?
Microsomal trig transfer protein (MTP)
111
What are examples of bacterial causes of infectious enterocolitis?
```
Cholera
Campylobacter enterocolitis
Shigellosis
Salmonellosis
Yersinia
E. coli
Pseudomembranous colitis
Whipple disease
```
112
What is indicative of cholera?
Rice water stools
113
What is the most common cause of bloody diarrhea?
Shigellosis
114
What organisms cause typhoid fever?
S. typhi and paratyphi
115
What is the morphology of typhoid fever?
Mucosal ulceration due to lamina propria inflammation
Lymphoid nodules in the liver
116
What species of Yersinia cause GI infections?
entercolitica and psuedotuberculosis
117
Symptoms of Yersinia infections mimic what?
Appendicitis
118
What are the different strains of E. coli and their characteristics?
Enterotoxigenic- traveller’s diarrhea
Enterohemorrhagic- shigella toxin, 0157:H7
Enteroinvasive- invades epithelial cells, acute limited colitis
Enteroaggregative-toxin with nonbloody diarrhea
119
What is pseudomembranous colitis often associated with?
Antibiotic use
120
What organism often cause pseudomembranous colitis?
C. difficile
121
What organism causes whipple disease?
Tropheryma whippelii
122
What is the morphology of whipple disease?
Shaggy mucosa (villi expansion)
Foamy macrophages stuffed with bacteria in the lamina propria
123
What are examples of viral causes of infectious enterocolitis?
Norovirus
Rotavirus
Adenovirus
124
What virus is commonly responsible for sporadic gastroenteritis in developing countries?
Norovirus
125
Rotavirus selectively infects and destroys what cells?
Mature enterocytes
126
What do small intestine biopsies of adenovirus reveal?
Epithelial degeneration or nonspecific villous atrophy and compensatory crypt hyperplasia
127
What are examples of parasitic causes of infectious enterocolitis?
```
Ascaris lumbricoides
Strongyloides
Negatory and Ancylostoma duodenale
Enterobius vermicularis
Trichuris trichuria
Schistosomiasis
Intestinal cestodes
Entamoeba histolytica
Giardia lamblia
Cryptosporidium
```
128
Strongyloides causes what kind of infection?
Autoinfection
129
What is the morphology of hookworms (Necator and Ancylostoma)?
Erosions and hemorrhage of the intestine
130
Trichuris infections cause what pathology?
Bloody diarrhea
Rectal prolapse
131
Where do the worms reside in Schistomiasis infections?
Mesenteric veins
132
What type of immune reaction is cause by Schistosomiasis infections?
Granulomatous
133
What do cestode infections not normally cause?
Eosinophilia
134
What is the morphology of ulcers produced in Entamoeba infections?
Flask-shaped
135
How do Cryptosporidium invade their hosts?
Organelle attaches to brush border and the enterocyte engulfs the organism
Lives in endocytic vacuole within the microvilli
136
How is IBS described?
Chronic, relapsing abdominal pain
Bloating
Changes in bowel habits
Normal gross and micro evaluation
137
What is IBD described as?
Chronic inappropriate mucosal immune activation
138
What are the two types of IBD and how are they differentiated?
1. Crohn disease-affects ileum and/or colon, skip lesions with transmural inflammation, wall is thick
2. Ulcerative colitis- only involves the colon, continuous lesions, mucosal inflammation, thin wall
139
Risk for developing colitis associated neoplasia is greater with what form?
Pancolitis
140
What are two causes of chronic colitis (besides IBD)?
1. Diversion colitis- blind distal segment after ostomy surgery
2. Microscopic colitis
141
What are the characteristics of diversion colitis?
Mucosal erythema and friability
Lymphoplasmacytic inflammation
Lymphoid follicular hyperplasia
142
What are the forms of microscopic colitis?
1. Collagenous colitis
| 2. Lymphocytic colitis
143
What is the most common finding in the intestine in GVHD?
Epithelial apoptosis
144
GVHD follows what kind of transplant?
Hematopoietic stem cell transplant
145
Why is sigmoid diverticulitis not considered true diverticuli?
Not invested in all three colonic wall layers
146
Sigmoid diverticulitis with no symptoms is termed what?
Diverticulosis
147
What is the morphology of sigmoid diverticulitis?
Flask-like outpouchings within a thin wall of flattened mucosa
Compressed submucosa
Attenuated/absent muscularis propria
148
What causes sigmoid diverticulitis?
Structure of colonic muscularis propria (taenia coli) and elevated intraluminal pressure in sigmoid colon
Exaggerated peristaltic contractions increases pressure
149
Where in the intestine are polyps most common?
Colo-rectal region
150
What is thought to be the cause of hyperplastic polyps?
Reduced epithelial cell turnover and delayed shedding
Goblet and absorptive cells “pile up”
151
Hyperplastic polyps resemble what other lesion?
Sessile serrated adenoma
152
Why must hyperplastic polyps and sessile serrated adenomas be distinguished?
Polyps don’t have malignant potential but the adenoma does
153
What are the histological features of inflammatory polyps?
Mixed inflammatory infiltrates
Erosion and epithelial hyperplasia
Lamina propria fibromuscular hyperplasia
154
Why may inflammatory polyps form?
Chronic cycles of injury and healing
Part of rectal ulcer syndrome
155
What is the triad of rectal ulcer syndrome?
1. Rectal bleeding
2. Mucus discharge
3. Inflammatory lesion of the anorectal sphincter
156
What is the morphology of juvenile hamartomatous polyps?
Pedunculated, smooth, reddish lesions with cystic spaces
Dysplasia rare
157
What increases the risk of developing cancer in juvenile hamartous polyps?
Autosomal dominant form with 3-300 lesions
158
What is Puetz-Jeghers syndrome and what are the characteristics?
Form of hamartomatous polyps
Multiple lesions
Mucocutaneous hyperpigmentation
Macules on lips, nostrils, buccal mucosa, palms, genitals and perianal region
Large, pedunculated polyps
159
How is Peutz-Jeghers syndrome differentiated from juvenile polyps?
Arborization
Presence of smooth muscle intermixed with lamina propria
160
What mutation causes Peutz-Jeghers syndrome?
Heterozygous loss of function in STK11
161
Neoplastic polyps are precursors to the majority of what disorders?
Colorectal adenocarcinomas
162
What is the most common neoplastic polyp?
Colonic adenoma
163
The risk of malignancy in neoplastic neoplasms is correlated to what?
Size
164
How are neoplastic polyps classified?
Tubular
Tubulovillous
Villous
165
What are two forms of neoplastic polyps and what are their characteristics?
1. Sessile serrated adenomas- lack cytologic dysplasia, serrated architecture throughout gland
2. Intramucosal carcinoma- dysplasia cells invade BM into lamina propria or muscularis mucosa
166
Which form of neoplastic polyps has little malignant potential?
Intramucosal carcinoma
167
What are the two kinds of familial polyploid syndromes?
1. Familial adenomatous polyposis (FAP)
| 2. Hereditary nonpolyposis colorectal cancer (HNPCC)/Lynch syndrome
168
How many polyps are required for the diagnosis of FAP?
100
169
What mutation causes FAP?
In adenomatous polyposis coli gene
170
Untreated, what is the risk of FAP developing into colon cancer by 30 years?
100%
171
What are two variants of FAP and what cancers are they associated with?
1. Gardner syndrome- osteomas, fibromatosis, epithelial cysts, duodenal and thyroid cancers
2. Turcot syndrome- medulloblastomas
172
What mutation is responsible for HNPCC and what does it cause?
In MSH 1 and 2 (responsible for DNA replication errors)
Microsatellite instability
173
What is the most common syndromic form of colon cancer?
HNPCC
174
What factors increase risk of developing HNPCC?
MMR mutations
CRC and endometrial cancers
175
What is the most common GI tract malignancy?
Adenocarcinoma
176
What is an uncommon site for adenocarcinoma in the GI tract?
Small bowel
177
What molecular events can lead to the colonic form of adenocarcinoma?
APC/beta catenin pathway and microsatellite instability pathway- beta cat aggregation activates genes that promote proliferation
Late K-RAS and p53 mutations promote growth and prevent apoptosis
SMAD mutations reduce TGF-B signalling (promote cell cycle)
Telomerase reactivation
178
What are the types of morphologies associated with colonic adenocarcinomas and what areas are they found in?
Proximal- polypoid, exophytic/bulky masses
Distal- anular/ring-like
Adenomas- tall columnar cell’s that resemble dysplastic epithelium
179
Invasive adenocarcinomas in the GI tract elicit what kind of response?
Strong desmoplastic/fibrotic response
180
Tumours that produce what substance have a worse prognosis?
Mucin
181
How are colonic tumours detected?
Cecal and right side- fatigue and weakness (IDA)
Left side- occult bleeding, changes in bowel habits/cramping, LLQ discomfort
182
What are the two most important prognostic factors in colonic adenocarcinomas?
Depth of invasion
Lymph node mets
183
What is the most common site of mets in colonic adenocarcinomas?
Liver
184
How do you differentiate between primary cancer and mets in the liver?
Mets- multiple lesions
Primary- one or two
185
What are the different forms of anal canal tumours and where are they found?
Upper third- columnar rectal epithelium (glandular)
Middle third- transitional epithelium (basaloid)
Lower third- stratified squamous epithelium (squamous)
186
Pure squamous cell is associated with what virus?
HPV
187
What are haemorrhoids?
Variceal dilations of anal and perianal submucosal venous plexi
188
What can cause rectal haemorrhoids?
Constipation
Venous stasis
189
What is the difference between external and internal rectal hemorrhoids?
External- ectasia of inferior hemorrhoid plexus below anorectal line
Internal- ectasia of superior hemorrhagic plexus above anorectal line
190
What does acute appendicitis present as?
Periumbilical pain
Migrated to RLQ
Nausea
Mild fever
Leukocytosis
191
What is the most common abdominal condition requiring surgery?
Acute appendicitis
192
The majority of acute appendicitis cases are associated with what?
Lumen obstruction
193
What are the characteristics of early and advanced acute appendicitis?
Acute- scant exudate, dull, granular and red serosa
Advanced- fibropurulent exudate, luminal abscess, ulceration, suppurative necrosis
194
What is the most common form of appendix tumours?
Carcinoid
195
Mucocele dilation of the appendix lumen can be caused by?
Benign obstruction
Adenoma
Adenocarcinoma
196
What is mucinous cystadenocarcinoma?
Appendiceal wall invasion by neoplastic cells which can lead to peritoneal implants
197
What is sclerosing retroperitonitis/Ormond disease?
Dense fibrosis of retroperitoneal tissue
198
Are peritoneal tumours benign or malignant?
Virtually all malignant
199
What are the causes of primary and secondary peritoneal tumours?
Primary- mesothelioma and desmoplastic small round cell tumour
Secondary- derived from any cancer (ovarian and pancreatic adenocarcinoma)
