GI TBP Flashcards

1
Q

2 main symptoms related to pathology of the GI tract

A

1) Abdominal pain

2) GI hemorrhage

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

Most frequent category/cause of chronic abdominal pain

A

Functional

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

Landmark that separates the upper GI tract from the lower GI tract

A

Ligament of Treitz

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

Pediatric congenital malformation that most commonly presents during adulthood or may remain asymptomatic throughout life

A

Meckel diverticulum

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

Congenital pyloric stenosis: Male vs female

A

Male

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

Congenital pyloric stenosis: Associated syndromes (2)

A

1) Turner

2) Trisomy 18

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

Congenital pyloric stenosis: Associated drug

A

Erythromycin

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

Duodenal atresia: Associated congenital anomaly

A

Trisomy 21 (Down syndrome)

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

Duodenal atresia: Symptom

A

Bilious vomiting in the first 24 hours of life

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

Duodenal atresia: Appearance on plain film (2)

A

1) Double-bubble sign

2) Paucity of gas distal to duodenum

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

Hirschprung disease: Males vs females

A

Males

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

Hirschprung disease: Common associated congenital anomaly

A

Trisomy 21 (Down syndrome)

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

Hirschprung disease: Pathogenesis

A

Aganglionosis of intestinal segment due to dysfunctional neural crest migration

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

Type of Hirschrpung that involves entire colon

A

Long-segment

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

Type of Hirschrpung that involves rectum and sigmoid

A

Short-segment

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

Hirschprung disease: Complication

A

Toxic megacolon

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

Intussusception: Triad

A

1) Colicky abdominal pain
2) Bilious vomiting
3) Currant jelly stools

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

Intussusception: PE

A

Sausage-shaped mass on the RUQ

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

Intussusception: Ultrasound

A

Target sign

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

Intussusception: Both a diagnostic and therapeutic intervention

A

Contrast enema

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

Meckel diverticulum: Persistent embryologic structure

A

Omphalomesenteric duct

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

Layers that are present in a true diverticulum

A

All layers of wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

T/F Most Meckel diverticula remain asymptomatic

A

T

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

Meckel diverticulum: Possible presentations

A

1) Intussusception
2) Obstruction
3) Bleeding (20%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Muscle layer deficient in a false diverticulum
Muscularis propria
26
What herniates in a false diverticulum
Mucosa
27
Most common cause of hematochezia in patients >60 years old
Colonic diverticulum
28
T/F Most diverticular bleeds are self-limited
T
29
Massive bleeding from a colonic diverticulum is best managed by (diagnostic and therapeutic)
Mesenteric angiography
30
Important rule for Meckel diverticulum (5)
Rule of Two's 1) 2% of the population 2) 2 inches long 3) 2 feet from ileocecal valve 4) Children younger than 2 y/o 5) 2 types of tissue (ectopic stomach or pancreas)
31
Grossly presents as white patches of hairy hyperkeratotic thickening on the lateral surface of the tongue
Hairy leukoplakia
32
Grossly presents as white patch on oral mucosa that cannot be scraped off
Leukoplakia
33
Microscopically, hyperparakeratosis, acanthosis, and "balloon cells" in the stratum spinosum
Hairy leukoplakia
34
Hairy leukoplakia vs leukoplakia vs SCC of oral cavity: Associated with immunosuppression
Hairy leukoplakia
35
Cause of hairy leukoplakia
EBV
36
80% of patients with hairy leukoplakia have this infection
HIV infection
37
T/F Leukoplakia can be premalignant
T
38
Major risk factor for leukoplakia
Tobacco use
39
Risk factor/s of SCC of oral cavity
Alcohol and tobacco use
40
Histology of 95% of head and neck tumors
SCC
41
T/F In salivary gland tumors, the larger the gland involved, the more likely it will be malignant
F
42
Most common parotid gland tumor
Pleomorphic adenoma
43
Risk factor for pleomorphic adenoma
Radiation
44
3 components of pleomorphic adenoma (microscopic)
1) Ductal cells 2) Myoepithelial cells 3) Matrix (myxoid, hyaline, chondroid)
45
Clinical presentation of pleomorphic adenoma
1) Slow-growing | 2) Painless
46
Benign vs malignant: Pleomorphic adenoma
Benign
47
Important surgical consideration for pleomorphic adenoma
High rate of recurrence if excised with no margins of neoplastic tissue
48
Carcinoma that can arise within a pleomorphic adenoma
Carcinoma ex pleomorphic adenoma
49
High vs poor: Survival rate in patients with carcinoma ex pleomorphic adenoma
Poor
50
Most common malignant tumor of the salivary glands
Mucoepidermoid carcinoma
51
65% of mucoepidermoid CA are found in what gland
Parotid
52
Condition whereby there is increased tone of the LES with subsequent failure to relax
Achalasia
53
In achalasia, there is loss of
VIP and NO inhibitory innervation of the LES
54
Secondary achalasia may arise from
1) Chagas disease 2) Malignancy 3) Sarcoidosis
55
Classic "bird's beak" appearance
Achalasia
56
Dysphagia initially to solids then progressing to liquids indicates
Mechanical problem
57
Dysphagia initially to liquids and then to solids indicates
Functional/motility problem
58
2 non-neoplastic disorders of the oesophagus associated with alcohol use
1) Mallory-Weiss tears | 2) Esophageal varices
59
Risk factors for Mallory-Weiss tears (2)
1) Alcoholism | 2) Hiatal hernia
60
Syndrome resulting from Mallory-Weiss laceration characterised by complete rupture of the esophagus
Boerhaave syndrome
61
Clinically presents as hematemesis after prolonged vomiting
Mallory-Weiss tears
62
Veins vs arteries: Esophageal varices
Veins
63
Mucosal vs submucosal: Esophageal varices
Submucosal
64
Refers to inflammation of the esophageal mucosa as a result of reflux of stomach contents
Reflux esophagitis or GERD
65
Complication of GERD that provides resultant risk of adenocarcinoma
Barrett esophagus or glandular metaplasia
66
Columnar glandular epithelium with goblet cells found in the esophagus
Barrett esophagus
67
Eosinophils, basal zone hyperplasia, and elongation of lamina propria papilla
GERD
68
Most common nonbacterial causes of esophagitis
1) CMV 2) HSV 3) Candida albicans
69
Common risk factor present in patients who have nonbacterial esophagitis
Decreased immune function
70
CMV vs HSV vs Candida albicans: Linear ulcers
CMV
71
CMV vs HSV vs Candida albicans: Punched out ulcers
HSV
72
CMV vs HSV vs Candida albicans: White plaque
Candida albicans
73
Glandular metaplasia that occurs in the distal esophagus as a result of chronic reflux of gastric acid into esophagus
Barrett esophagus
74
T/F: Glandular metaplasia in the oesophagus may be reversible
T
75
Lifetime risk for development of oesophageal adenoma in patients with Barrett esophagus
10%
76
Nonbacterial esophagitis seen microscopically as squamous cells with intranuclear inclusions with a clear halo
HSV
77
Microscopic finding in HSV infection described as squamous cells with intranuclear inclusions with a clear halo
Cowdry type A HSV inclusions
78
T/F Esophageal webs are always congenital
F
79
Syndrome associated with esophageal webs
Plummer-Vinson
80
Tetrad of Plummer-Vinson syndrome
1) Esophageal webs 2) IDA 3) Glossitis 4) Cheilosis
81
T/F Plummer-Vinson syndrome carries a risk for malignancy
T
82
Esophageal ring located above the squamocolumnar junction
Type A
83
Type B esophageal ring is also known as
Schatzki ring
84
Esophageal ring located at the squamocolumnar junction
Type B
85
Clinical presentation of webs and rings
Intermittent dysphagia
86
Type of false esophageal diverticula: Located at the proximal esophagus
Zenker
87
Type of true esophageal diverticula: Located at mid esophagus
Traction
88
Type of true esophageal diverticula: Located near the GE junction
Epiphrenic
89
Autoimmune disease that can cause oesophageal stenosis
Scleroderma
90
Most common type of esophageal CA worldwide
SCC
91
Male vs female: SCC of esophagus
Male
92
SCC of esophagus: Most common location
Middle 3rd (Robbin's)
93
SCC of esophagus: Risk factors
1) Smoking and alcohol use 2) Dysphagia 3) Plummer-Vinson syndrome 4) Vitamin A deficiency
94
SCC of esophagus: Upper third SCC spreads to
Cervical LN
95
SCC of esophagus: Middle 3rd SCC spreads to
Mediastinal, paratracheal, and tracheobronchial LN
96
SCC of esophagus: Lower 3rd SCC spreads to
Gastric and celiac LN
97
AdenoCA of esophagus: Male vs female
Male
98
AdenoCA of esophagus: Whites vs African Americans
Whites
99
SCC of esophagus: Whites vs African Americans
African Americans
100
AdenoCA of esophagus: Occurs almost exclusively with
Barrett esophagus
101
AdenoCA of esophagus: Most common location
Distal esophagus
102
AdenoCA of esophagus: Rare source
Submucosal glands
103
T/F In esophageal neoplasms, by the time symptoms are present, most tumours are incurable
T
104
Role of prostaglandin in gastric mucosal integrity
1) Mucus production | 2) Bicarbonate secretion
105
2 main type of chronic gastritis
1) Type A or fundal | 2) Type B or antral
106
Etiology of fundal chronic gastritis
Autoimmune disease
107
Etiology of antral chronic gastritis
H. pylori
108
Mechanisms by which H. pylori damages gastric mucosa
1) IL-8 (chemotaxin) 2) Urease (urea->ammonia->buffers HCl) 3) Enhancement of gastric acid and impairment of HCO3 4) Epithelial adherence and secretion of phospholipases and proteases 5) VacA (passive urea transporter causing vacuolization)
109
In H. pylori infection, VacA requires the presence of
CagA gene
110
Extensive loss of parietal cells: H. pylori gastritis vs autoimmune gastritis
Autoimmune
111
Achlorhydria: H. pylori gastritis vs autoimmune gastritis
Autoimmune
112
Noninvasive testing for H. pylori (3)
1) Serology 2) Urea breath test 3) Stool Ag test
113
Invasive testing for H. pylori
1) Biopsy urease test 2) Culture 3) Histology
114
Other names for autoimmune gastritis (2)
1) Atrophic gastritic | 2) Pernicious anemia
115
Mechanism of autoimmune gastritis
Antibodies to parietal cells results in decreased gastric acid secretion and IF production
116
Anemia associated with autoimmune gastritis
Megaloblastic
117
Vitamin deficiency associated with autoimmune gastritis
Vitamin B12
118
Autoimmune disorder associated with autoimmune gastritis
Hashimoto thyroiditis
119
Storage disorder that may cause chronic gastritis
Amyloidosis
120
Most common cause of gastric and duodenal ulcers
H. pylori infection
121
Second most common cause of gastric peptic ulcers
NSAIDs
122
Most common complication of PUD
GI bleeding
123
T/F Most patients with peptic ulcers have normal acid secretion
T
124
Syndrome associated with gastrin-secreting tumor
Zollinger-Ellison syndrome
125
Zollinger-Ellison syndrome: Location of tumor
Gastrinoma triangle, at the 2nd and 3rd portions of duodenum, at the junction of the head and neck of the pancreas, and the cystic duct
126
Most gastrin-secreting tumors are: Sporadic vs component of MEN 1
Sporadic
127
PUD vs gastric adenoCA ulcer: Punched out, edges not piled up
PUD
128
PUD vs gastric adenoCA ulcer: Heaped up edges
Gastric adenoCA
129
Acute gastric ulcer caused by severe stress
Cushing ulcer
130
Acute gastric ulcer caused by burns
Curling ulcers
131
Cause of acute gastric ulcer in patients with head trauma
Increased ICP produces increased vagal stimulation resulting in excess gastric acid production
132
Cause of acute gastric ulcer in shock and septic patients
Reperfusion injury due to greater than physiologic amounts of nitric oxide
133
Most common gastric neoplasms
AdenoCA
134
Most common type of gastric polyps: Hyperplastic vs adenomatous
Hyperplastic
135
2 types of gastric adenocarcinoma under the Lauren classification
1) Intestinal | 2) Diffuse
136
Intestinal gastric adneocarcinoma: Male vs female
Male
137
Intestinal gastric adenocarinoma: Greater vs less than 50 y/o
Greater
138
Intestinal vs diffuse gastric adenoma: Arises from a precursor lesion, eg intestinal metaplasia in the background of chronic gastritis
Intestinal
139
Intestinal gastric adenoCA: Risk factors
1) Nitrites 2) Cigarette smoke 3) Chronic gastritis with intestinal metaplasia
140
Intestinal vs diffuse gastric adenoCA: Depth of invasion into the wall is vital to staging
Intestinal
141
Early gastric adenoCA invades
Submucosa
142
Late gastric adenoCA invades
Muscular wall
143
Diffuse gastric adenoCA is aka
Signet-ring cell type
144
Diffuse gastric adenoCA: Male vs female
No preponderance
145
Diffuse gastric adenoCA: Younger vs older than 50 y/o
Younger
146
Diffuse gastric adenoCA: Risk factors
Unknown
147
Diffuse gastric adenoCA: Gross finding
Linitis plastica or thickening of wall
148
Diffuse gastric adenoCA: Microscopic finding
Signet-ring cell (eccentric nucleus with vacuole)
149
Refers to gastric adenoCA metastasis to supraclavicular LN
Virchow's node
150
Refers to gastric adenoCA metastasis to periumbilical nodule
Sister Mary Joseph nodule
151
GISTs are derived from
Interstitial cells of Cajal
152
Increase in stool mass, frequency, or fluidity
Diarrhea
153
In diarrhea, stool weight exceeds:
200g within 24h
154
Low volume, painful, bloody diarrhea often due to infectious organisms
Dysentery
155
Causative entities: Secretory diarrhea (3)
1) Rotavirus 2) Norwalk virus 3) Vibrio cholerae 4) Bacillus cereus 5) Giardia lamblia
156
Causative entities: Osmotic (2)
1) Disaccharidase deficiency | 2) Lactulose therapy
157
Causative entities: Exudative (4)
1) Shigella 2) Salmonella 3) Campylobacter 4) IBD
158
Causative entities: Malabsorption (2)
1) Celiac sprue | 2) IBD
159
Causative entities: Altered motility (2)
1) DM | 2) Hyperthyroidism
160
Type of diarrhea: Isotonic fluid secretion that persists with fasting
Secretory
161
Type of diarrhea: Solutes in the bowel draw fluid to lumen
Osmotic diarrhea
162
Type of diarrhea: Damage to epithelial layer by cytotoxins or invasion of mucosa usually caused by bacterial organisms
Exudative diarrhea
163
Type of diarrhea: Due to a defect in digestion (absence of enzyme or decreased surface area) increases osmolality of luminal contents, thereby drawing water into the bowel
Malabsorption
164
Type of diarrhea: Improves with fasting
Osmotic diarrhea
165
Amount of stool in high output secretory diarrhea
>1L per day
166
Stool osmotic gap in high output secretory diarrhea
Minimal (
167
Stool osmotic gap in osmotic diarrhea
Elevated
168
Diarrheal complication occurring from drinking nonsterilized water from creeks and streams
Giradiasis
169
Complications-associated diarrhea: Metabolic acidosis, dehydration
Secretory
170
Complications-associated diarrhea: Dehydration, sepsis, perforation
Exudative
171
Duration: Acute diarrhea
172
Duration: Chronic diarrhea
>4 months
173
Proximal vs distal intestinal disease: Large volume
Proximal
174
Proximal vs distal intestinal disease: Urgency
Distal
175
Organism that affects the distal colon, causing inflammation, erosions, exudates, and ulcers
Shigella
176
Organism that affects the ileum and colon, causing oval-shaped ulcers along the axis
Salmonella
177
Pseudomembranous colitis: Organism
C. difficile
178
Pseudomembranous colitis: Pathogenesis
Antibiotic use kills normal gut flora allowing normal inhabitant, C. difficile, to proliferate and produce toxin
179
Pseudomembranous colitis: Onset
1 week after initiation of antibiotic therapy
180
Pseudomembranous colitis: Diagnosis (2)
1) C. difficile antigen in stool | 2) Endoscopy and biopsy
181
Other causes of pseudomembranes (3)
1) Ischemia 2) Staph 3) Shigella
182
Entamoeba histolytica infection: Mechanism
Crypt invasion into submucosa
183
Entamoeba histolytica infection: Complication
Invade into portal vessels and embolize liver, lung, heart, brain, and kidneys
184
Entamoeba histolytica infection: Gross (2)
1) Flask-shaped ulcer in colon | 2) Anchovy paste-like mass in liver
185
Entamoeba histolytica infection: Microscopic
Amoebae with engulfed RBCs
186
Characteristic of entamoeba that confirms pathogenicity
Engulfed RBCs
187
Pseudomembranous colitis: Gross
Adherent green-tan membranes on mucosal surface of colon
188
Pseudomembranous colitis: Components of pseudomembrane
1) Epithelial cells 2) Inflammatory cells 3) Fibrin
189
Causes of malabsorption-associated mechanism: Pancreatic insufficiency, defective blue secretion
Impaired intraluminal digestion
190
Causes of malabsorption-associated mechanism: Lactose intolerance
Primary mucosal cell abnormality
191
Causes of malabsorption-associated mechanism: Bacterial overgrowth
Primary mucosal cell abnormality
192
Causes of malabsorption-associated mechanism: Celiac sprue
Reduced surface area
193
Causes of malabsorption-associated mechanism: IBD
Reduced surface area
194
Causes of malabsorption-associated mechanism: Lymphoma
Lymphatic obstruction
195
Causes of malabsorption-associated mechanism: Tuberculosis
Lymphatic obstruction
196
Causes of malabsorption-associated mechanism: Enterocolitis
Infections
197
Causes of malabsorption-associated mechanism: Crohn's disease
Reduced surface area
198
Malabsorption clinically presenting as bloating and soft diarrheal movements
Carbohydrate malabsorption
199
Presence of D-xylose in urine indicates
Adequate intestinal transport and surface area
200
Normal D-xylose test warrants
Other tests of malabsorption
201
Abnormal D-xylose test warrants
Intestinal biopsy
202
Schilling test is for the diagnosis of
Vitamin B12 deificiency
203
Substances administered in Schilling test
1) Radioactive vitamin B12 2) Oral IF 3) Antibiotics 4) Pancreatic enzymes
204
Where radioactive vitamin B12 is measured in Schilling test
Urine
205
Diagnosis if deficiency is corrected with administration of oral IF
Pernicious anemia
206
Diagnosis if deficiency is corrected with administration of antibiotics
Bacterial overgrowth
207
Diagnosis if deficiency is corrected with administration of pancreatic enzymes
Pancreatic insufficiency
208
Pathogenesis-associated cause of malabsorption: Gluten hypersensitivity
Celiac sprue
209
Pathogenesis-associated cause of malabsorption: Disaccharidase deficiency
Lactose intolerance
210
Pathogenesis-associated cause of malabsorption: Possible dysfunction of immune response toward normal intestinal flora
IBD
211
Pathogenesis-associated cause of malabsorption: G+ Tropheryma whippelii
Whipple's disease
212
Celiac sprue is associated with the development of what neoplasms
1) SCC of esophagus 2) Small intestinal adenoCA 3) Intestinal T-cell lymphoma
213
Disease entity associated with overgrowth of E. coli or haemophilus involving the entire small intestine
Tropical sprue
214
T/F Tropical sprue carries a risk for developing lymphoma
F
215
Malabsorptive diseases associated with flattened villi, lymphocytic infiltrates, and crypt hyperplasia in the small intestine
Celiac sprue
216
Tropical vs celiac sprue: Changes worse in the duodenum and proximal SI
Celiac sprue
217
T/F Extraintestinal manifestations are common in celiac sprue
T
218
Classic extra intestinal manifestations of celiac sprue (2)
1) Dermatitis herpetiformis | 2) Prupritic papular and vesicular rash on EXTENSOR surfaces and buttocks
219
Lactose intolerance: Asians vs Americans
Asians
220
Lactose intolerance: Childhood vs adulthood
Adulthood
221
Lactose intolerance: Byproduct of lactose breakdown (gas)
Hydrogen
222
UC vs CD: Confined to mucosa
UC
223
UC vs CD: Transmural
CD
224
UC vs CD: Higher risk of colonic adenoCA
UC
225
Most common extra intestinal manifestation of Crohn disease
Migratory polyarthritis
226
Urinary crystals associated with CD
Calcium oxalate
227
Form of UC NOT associated with increased risk for carcinoma
Proctitis
228
UC vs CD: Serpentine ulcers
CD
229
UC vs CD: Crypt abscesses
UC
230
UC in barium enema
Loss of haustra
231
CD in barium enema
String sign
232
Whipple disease: Male vs female
Male
233
Whipple disease: Primary organs affected (3)
1) Intestines 2) CNS 3) Joints
234
Whipple disease: Microscopic
PAS-positive macrophages in lamina propria
235
T/F: Whipple disease may cause blindness
T
236
Compressed by volvulus: Venous drainage vs arterial supply
Venous drainage
237
Transmural vs mural vs mucosal infarct: Ischemic bowel due to occlusion of vessel
Transmural
238
Transmural vs mural vs mucosal infarct: Ischemic bowel due to hypoperfusion
Mural and mucosal
239
2 phases of hypoperfusion injury
1) Hypoxic injury | 2) Reperfusion injury
240
Phase of hypo perfusion injury in which most damage occurs
Reperfusion injury
241
Characteristic symptom of patients with ischemic bowel disease
Abdominal pain out of proportion to PE findings
242
Abdominal pain out of proportion to PE findings is due to
Mesenteric infarction
243
Diagnosis of ischemic bowel disease is confirmed with
Angiography
244
True vs false diverticulum: Meckel diverticulum
True
245
Dilation of submucosal and mucosal blood vessels in elderly individuals that can cause massive painless hematochezia
Angiodysplasia
246
Condition characterized by many diverticuli
Diverticulosis
247
False diverticula of intestine is most commonly seen in which segment
Descending colon and rectum
248
Causes of apple-core lesion on barium enema (2)
1) Adenocaricnoma of colon | 2) Thickened false diverticulum
249
Majority of intestinal obstructions are caused by (2)
1) Adhesions | 2) Hernias
250
Causes of pseudo-obstruction of intestines
1) Paralytic ileus | 2) Ischemic bowel disease
251
Tubular vs villous vs tubulovillous adenoma: More prone to malignant degeneration
Villous
252
Hamartomatous polyps in the small intestine that include the muscular is mucosa
Peutz-Jeghers polyps
253
Size of villous adenoma that has greatly increased risk of harbouring a malignant neoplasm
>4.0 cm
254
Disease entity characterised by the presence of hundreds of adenomas in the colon
Familial adenomatous polyposis (FAP)
255
FAP: Gene mutation
APC gene
256
Normal APC gene promotes
Degradation of b-catenin
257
FAP: Inheritance pattern
Autosomal dominant
258
FAP: Risk of progression to invasive adenoma by age 50
100%
259
FAP: Treatment
Colectomy
260
T/F HNPCC is characterised by increased number of polyps in the GIT
F
261
Ascending vs descending colon: Present sooner by causing more of an obstruction
Descending
262
Ascending vs descending colon: Present later because they do not cause an obstruction
Ascending
263
T/F AdenoCA is common in the small intestine
F
264
T/F Depth of invasion into the wall is not important in staging of adenoCA
F
265
Most common site of metastasis of colon adenoCA
Liver
266
Ascending vs descending colon: Pain
Descending
267
Ascending vs descending colon: IDA
Ascending
268
Ascending vs descending colon: Change in stool caliber
Descending
269
Ascending vs descending colon: Occult bleeding
Ascending
270
Ascending vs descending colon: Apple-cire on barium enema
Descending
271
Ascending vs descending colon: Exophytic mass
Ascending
272
Ascending vs descending colon: Infiltrating mass
Descending
273
Earliest sign of colonic adenoCA
Occult bleeding
274
T/F All anemia patients >50 is considered colon CA until proven otherwise
T
275
Carcinoid tumor: Location
1) Ileum 2) Appendix 3) Rectum 4) Bronchi
276
Rule of carcinoid tumor
1/3 1) Metastasize 2) Present with a second malignancy 3) Have multiple tumors
277
Carcinoid syndrome is produced by carcinoid tumour due to release of
Serotonin
278
Carcinoid timor takes place when carcinoid timor metastasise to
Liver
279
Most common valve involved in carcinoid synrome
Tricuspid
280
T/F Carcinoid tumours are high grade
F
281
Characteristic appearance of nucleus of cells in carcinoid tumors
Salt and pepper nucleus