GI Pathology (10.1 - 10.6) Flashcards
1
Q
What is the cause of cleft lips/ palate?
A
failure of the facial prominences to fuse
2
Q
True or false: cleft lip and palate usually occur together
A
True
3
Q
How do the pharyngeal arches fuse in development?
A
Come from all directions to fuse together to form the mouth
4
Q
Superficial ulcerations of the oral mucosa = ?
A
Aphthous ulcer
5
Q
What are the gross characteristics of aphthous ulcers?
A
Grayish base surrounded by erythema (granulation tissue)
6
Q
What is Behcet syndrome? What causes it? What is the classic triad of symptoms?
A
Recurrent aphthous ulcers, genital ulcers, and uveitis caused by immune complex vasculitis of small vessels
7
Q
When do the symptoms of Behcet syndrome usually recur?
A
After viral infection
8
Q
What is the virus that usually causes oral herpes?
A
HSV-1
9
Q
What are the gross characteristics of oral herpes?
A
Shallow, painful red ulcers or vesicles on the lips
10
Q
When in life does HSV-1 infection usually occur? Where does it lie dormant?
A
Early in childhood, and remains dormant in the ganglia in the trigeminal nerve
11
Q
What causes the reactivation of the HSV-1 virus?
A
Stress and sunlight
12
Q
What is the most common location of SCC in the mouth?
A
Floor of the mouth
13
Q
What are the risk factors for developing SCC in the mouth?
A
EtOH and Tobacco
14
Q
What are the precursor lesions to SCC in the oral cavity?
A
Leukoplakia or erythroplakia
15
Q
What is the risk of leukoplakia/erythroplakia?
A
Progression to SCC
16
Q
What are the diseases that should be in your differential when you see white plaques in the oral cavity? How do you differentiate?
A
Oral candidiasis
Hairy Leukoplakia
Leukoplakia
Scrape it off (candida if it comes off)
17
Q
Where is hairy leukoplakia usually found? What virus causes this?
A
Lateral aspect of the tongue
EBV
18
Q
What are the two major differences between oral hairy leukoplakia, and leukoplakia of SCC?
A
Oral hairy leukoplakia is caused by EBV, and is only hyperplasia of the tongue cells
SCC leukoplakia is dysplasia
19
Q
—-What is erythroplakia? What does this suggest?—-
A
—-Leukoplakia that is vascularized
this suggests squamous dysplasia—–
20
Q
What are the three major salivary glands in the mouth?
A
- Parotid
- Submandibular
- Sublingual
21
Q
What is the most feared complication of mumps? Why?
A
Sterility secondary to testicular infection
22
Q
What is the virus that causes mumps? Family?
A
- Mumps virus
- Paramyxovirus
23
Q
What are the two causes of increased serum amylase in Mumps?
A
Increased production from BOTH the salivary gland, and pancreas
24
Q
What GI organ can be affected with Mumps? What does it cause?
A
Pancreatitis
25
What are the neurological concerns with Mumps?
Meningitis
26
What is sialadenitis? What is the usual cause? What is the feared complication of this?
Inflammation of the salivary gland usually secondary to sialolithiasis and subsequent Staph. Aureus infection
27
True or false: Sialadenitis is usually bilateral
False- usually unilateral
28
What is pleomorphic adenoma? What are the tissue types that compose this?
Benign salivary gland tumor composed of stromal and epithelial tissue
29
Where do pleomorphic adenoma usually occur?
Parotid gland
30
What are the s/sx of pleomorphic adenomas?
Mobile, painless circumscribed mass at the angle of the jaw
31
What nerve is at risk with parotid gland tumors?
Facial nerve issues
32
Why is there a high rate of recurrence of pleomorphic adenomas?
Very irregular margins, thus may lead to leaving in cells during a surgery
33
What is a Warthin tumor? Histological characteristic?
Benign cystic tumor with abundant *lymphocytes and germinal centers*
34
Where do Warthin tumors usually arise? Why?
Parotid glands--one of the last glands in development to separate from adjacent lymph node tissues
35
What are the benign tumors of the parotid gland? (3)
- Pleomorphic adenomas
- Warthin tumors
- Mucoepidermoid carcinoma
36
What is the most common malignant tumor of the parotid gland?
Mucoepidermoid carcinoma
37
-----What are mucoepidermoid carcinomas? What type of cells compose it? Where is it usually found?-----
-----Malignant tumor composed of mucinous and squamous cells that usually arises in the parotid gland-----
38
What is the most common congenital defect of the esophagus?
Atresia of the esophagus, with a fistula between the distal esophagus and the trachea
39
What are the signs of esophageal atresia in utero (1), and when born (2)?
- Polyhydramnios
- Abdominal distention
- Aspiration
40
What are esophageal webs? What layer of the esophagus is involved, and where in the esophagus do these usually occr?
Thin protrusion of esophageal mucosa, most often in the upper esophagus
41
What are the signs of esophageal webs? What cancer are these patients predisposed to?
- Dysphagia for poorly chewed foods
| - SCC
42
What causes the abdominal distention and aspiration with esophageal atresia?
-Air going into the stomach causes distention, with resulting regurgitation going into the trachea and lungs
43
What are the four layers of the GI tract?
- Mucosa
- Submucosa
- Muscularis propria
- Serosa
44
What is the most common complication of esophageal webs?
Plummer-Vinson syndrome
45
What is Plummer-Vinson syndrome? What is the classic triad of symptoms?
Severe Fe deficiency anemia presenting with:
- beefy red tongue
- dysphagia
- Fe deficiency anemia
46
What is a Zenker diverticulum? Where does this usually occur?
Out pouching of pharyngeal mucosa through an *acquired* defect in the muscular wall, arising above the upper esophageal sphincter at the junction of the esophagus and pharynx
47
What are the s/sx of a Zenker diverticulum? (3)
- Dysphagia
- obstruction
- halitosis
48
What layers of the GI tract are involved in a Zenker diverticulum? Is this a true diverticulum?
Pharyngeal mucosa and submucosa--no, since it does not involve the muscularis externa
49
What is Mallory-Weiss syndrome? Cause?
Longitudinal laceration of the mucosa at the gastroesophageal junction, d/t excessive vomiting (alcoholism, and bulimia)
50
What are the s/sx of Mallory-Weiss syndrome?
**Painful** hematemesis
51
What disease can Mallory-Weiss syndrome progress to?
Boerhaave syndrome
52
What is Boerhaave syndrome?
Rupture of the esophagus, causing air in the mediastinum and subcutaneous emphysema of the neck
53
What is the cause of esophageal varices?
Portal HTN
54
What are the two veins that the esophageal vessels drain into?
- Azygos vein into the SVC
| - Left gastric into the hepatic portal
55
What is the cause of painful hematemesis? Painless?
Painful = Mallory-Weiss syndrome
Painless = esophageal varices
56
What are the two major reasons esophageal varices 2/2 portal HTN results in profuse hemorrhaging?
- Increased probability of rupture
| - Lower coag factors d/t cirrhosis
57
What is achalasia? What is the cause of this?
- Disordered esophageal motility with inability to relax LES
| - Due to damaged ganglion cells in the myenteric nerve plexus
58
What parasitic infection can lead to achalasia of the esophagus?
Chagas disease
59
What are the s/sx of achalasia (2)? Imaging findings?
- Inability to swallow solid *and* liquids
- Halitosis
- "Bird Beak" sign of the esophagus on Ba swallow
60
What is the plexus of nerves that runs between the inner circular layer, and outer longitudinal layer of the GI tract? What is the function of this plexus?
- Myenteric
| - Controls muscle motility
61
What neoplastic process can achalasia progress to?
esophageal SCC
62
What is the relative pressure of the LES in achalasia (high or low)?
High
63
What is the change in the cell type of Barrett's esophagus secondary to GERD?
*non-Keratinized stratified squamous* to *non-ciliated simple columnar with goblet cells*
64
What are the two major causes of GERD?
- Hiatal hernia
| - lower LES pressure
65
What are the two types of hiatal hernias?
- Sliding (cardia of the stomach protrudes into the esophagus)
- Paraesophageal (stomach herniates next to the esophagus in the diaphragm)
66
What is the appearance of a sliding hiatal hernia on Ba swallow?
Hourglass appearance
67
What is the classic physical exam sign of paraesophageal hiatal hernias?
Bowel sounds in the thorax
68
How does GERD cause asthma and cough?
Irritation of the airways from reflux
69
What are the dental findings of GERD?
Increased acid = damaged enamel
70
Where are the stem cells in the layers of the stomach? What is the significance of this in relation to GERD?
Mucosa--if knock out the mucosa, then will heal by fibrosis, causing a loss of the tone present in the LES
71
What is the most common type of esophageal cancer in the West? What is this usually associated with? Where in the esophagus does this usually occur?
- Adenocarcinoma
- Barrett's esophagus
- Distal 1/3
72
What is the most common esophageal cancer *worldwide*? Where in the esophagus does this usually arise?
- SCC
| - upper or middle third of the esophagus
73
What is the cause of SSC of the esophagus?
Irritation of the esophagus
74
How do Achalasia and esophageal webs lead to SCC?
Irritation via food degradation sitting in the esophagus
75
What are the s/sx of SCC of the esophagus? (3)
- Progressive dysphagia
- Hematemesis
- Hoarse voice/cough
76
-----Where does lymph flow in the upper 1/3 of the esophagus? Middle? Distal?-----
- -----Upper = cervical nodes
- Middle = mediastinal or tracheobronchial nodes
- Lower = celiac and gastric nodes------
77
Why is it that esophageal SCC can present with hoarse voice?
Invasion of the SCC beyond the BM may lead to compression of the recurrent laryngeal nerve
78
What is gastroschisis?
Congenital malformation of the abdominal wall, causing an exposure of abdominal contents
79
What is an omphalocele?
Persistent herniation of bowel into the umbilical cord, due to failure of herniated intestines to return to the body cavity during development
80
What comprises the cover of omphaloceles? How about in a gastroschisis?
- Peritoneum and amnion of the umbilical cord
| - Nothing for a gastroschisis
81
What way does the intestines rotate during development, when it is in the umbilical yolk stalk?
Counterclockwise 270 degrees
82
What is the cause of pyloric stenosis? Which gender is this more common in?
- Hypertrophy of the pyloric smooth muscle
| - Males
83
When does the pyloric stenosis usually form relative to birth? What are the s/sx?
- 2 weeks *after* birth
| - *Non-bilious* projectile vomiting and olive-like mass in the abdomen
84
What is the treatment for pyloric stenosis?
Myotomy of the pyloric sphincter
85
What is acute gastritis? What are the two ways in which this occurs?
Increase acid production or decreased mucosal protection in the stomach, causing degradation of the stomach by acid
86
What are the two type of chronic gastritis?
- Chronic autoimmune gastritis
| - Chronic H.Pylori gastritis
87
What are the three major components of mucosal protection from stomach acid? (3)
- Mucus (foveolar cells)
- Bicarb secretion
- Blood flow (picks up acid)
88
What are Curling ulcers?
Stomach ulcers in the context of a severe burn d/t hypovolemia and lower blood flow to the stomach.
89
What is a cushing ulcer?
Increased intracranial pressure, causing increased vagal stimulation, and increased ACh, which increases acid production
90
What are the effects of prostaglandins on the stomach? (3)
- Increase mucus and bicarb secretion from foveolar cells
- Decrease acid secretion
- Increase blood flow to the stomach to sweep away acid
91
What are the three receptors on parietal cells in the stomach that lead to increased acid secretion?
- Histamine (paracrine)
- ACh (neurotransmitter)
- Gastrin (Endocrine)
92
What is the cell in the stomach that creates acid? What other important protein does this secrete?
- Parietal cell
| - Intrinsic factor
93
What is the MOA of shock causing ulcers?
Hypovolemia causes decreased blood flow to the stomach lining
94
What are the three outcomes of acid damage in the stomach, and how are each of these defined?
- Superficial inflammation
- Erosion (loss of epithelial layer)
- Ulceration (loss of mucosal layer)
95
What is the pathophysiology of chronic autoimmune gastritis? What type of hypersensitivity reaction is this? What is the significance of the antibodies produced in this?
Autoimmune destruction of parietal cells (and/or intrinsic factor). This is a type IV hypersensitivity rxn
-Antibodies are a consequence of the damage, not the cause of it
96
What are the two places in the stomach that parietal cells are common in?
- Fundus
| - Body
97
What is the achlorhydria seen in chronic autoimmune gastritis?
Lack of acid production secondary to loss of parietal cells
98
What happens to acid levels, gastrin levels, and G cells in chronic autoimmune gastritis?
- Decrease acid
- Increased gastrin
- Antral G cell hyperplasia
99
Pernicious anemia has a high or low MCV?
High
100
What is the most common cause of vitamin B12 deficiency? What is this disease called?
- Autoimmune chronic gastritis
| - Pernicious anemia
101
Why are pts with chronic, autoimmune gastritis at an increased risk for gastric adenocarcinoma?
Chronic irritation / inflammation induces metaplasia of the foveolar cells with goblet cell formation
102
What is the most common cause of chronic gastritis?
H.Pylori infx
103
What are the two enzymes that H. Pylori secretes that allow it to live on the stomach lining?
- Urease
| - Proteases
104
What is the most common site of H.Pylori infection?
Antrum of the stomach
105
Does H.Pylori invade the stomach mucosa?
No
106
Why are pts with chronic gastritis at an increased risk for MALT lymphoma?
generation of germinal center and post germinal center B cells from the MARGINAL zone
107
What is the treatment for gastric carcinoma/MALT lymphoma secondary to H.Pylori infection?
Triple therapy (PPI, Az, Clindamycin)
108
What are the two ways in which you could confirm that the treatment for H.Pylori was effective?
- Negative urea breath test
| - No H.Pylori antigen in the stool
109
What is the most common site of peptic ulcers?
Proximal duodenum
110
What is the major cause of PUD?
H.Pylori infection
111
What are the s/sx of duodenal PUD?
Epigastric pain that *improves* with meals
112
What is Zollinger-Ellison syndrome?
CA of the gastrin secreting portions of the stomach, causing increased acid release and ulcer formation
113
Why are the symptoms of PUD improved with meals?
Duodenum will increased HCO3 secretion, neutralizing the acid
114
What is the most common complications of PUD rupture?
Rupture of the walls of the duodenum
115
What happens if there is a rupture of the *anterior* wall of the duodenum?
Air beneath the diaphragm
116
What happens if there is a rupture of the *posterior* wall of the duodenum? (What organ and artery are at risk)?
- Acute pancreatitis
| - Gastroduodenal artery rupture
117
Why is it that gastric ulcer symptoms worsen with meals?
increased acid secretion
118
What are the two most common causes of gastric ulcers?
- NSAID use
| - H. Pylori
119
What artery is at risk if a gastric ulcer ruptures along the lesser curvature of the stomach?
Left gastric artery
120
True or false: duodenal ulcers are almost never malignant?
True
121
What are the gross characteristics of a non-cancerous ulcer in the stomach?
Flat. small, with well defined borders
122
What are the gross characteristics of a cancerous ulcer in the stomach?
Large, irregular and piled up borders
123
Gastric carcinoma is a malignant proliferation of what cells? What type of cancer, then, does this lead to?
Surface epithelial cells (adenocarcinoma)
124
What are the two general types of gastric carcinomas?
- Intestinal
| - Diffuse
125
What are the features of the intestinal type of ulcer?
large, irregular ulcer with heaped up margins
126
Where are intestinal gastric carcinomas usually found in the stomach?
Along the lesser curvature of the antrum
127
What are the 3 risk factors for intestinal type gastric carcinoma? (food chemicals, blood type, etc)
- Nitrosamines
- Blood type A
- Intestinal metaplasia
128
What are the histological characteristics of diffuse type gastric carcinomas?
Signet rings cells that diffusely infiltrate the gastric wall
129
What causes the thickening of the stomach wall in diffuse type gastric carcinoma? What is this called?
- Desmoplasia
| - Linitis plastica
130
True or false: The diffuse type of gastric carcinoma is not associated with H.Pylori infx, metaplasia, or nitrosamines
True
131
What are the s/sx of gastric carcinoma? (besides pain and weight loss) (4)
- Early satiety
- Anemia
- Abdominal pain
- Weight loss
132
What is the Leser-Trelat sign? What GI malignancy is this seen in?
The Leser-Trélat sign is the explosive onset of multiple seborrheic keratoses often with an inflammatory base.
This can be seen with Gastric carcinoma!
133
Distant mets from gastric carcinomas usually involve what organ?
- Liver
- Periumbilical region
- Bilateral ovaries
134
What is the sister Mary Joseph nodule?
mets from gastric CA to the periumbilical region
135
----What is the Krukenberg tumor?----
----Bilateral mets from gastric CA to the ovaries----
136
What is duodenal atresia?
failure of the small bowel to canalize
137
What genetic disease is duodenal atresia associated with?
Down syndrome
138
What are the s/sx of duodenal atresia? (3, in utero and postpartum)
- Polyhydramnios
- Double bubble sign
- Bilious vomiting
139
What is the vomiting like in pyloric stenosis? Duodenal atresia?
- Pyloric stenosis = non-bilious
| - Duodenal atresia = bilious
140
What is Meckel diverticulum? Is this a true diverticulum?
true diverticulum that arises due to a failure of vitelline duct to involute
141
What is the vitelline duct?
Pathway that receives nutrients from the yolk sac during development
142
Passing of meconium via the umbilicus at birth = ?
Failure of the vitelline duct to involute
143
Soft stool in the periumbilical region of an infant's abdomen = ?
Meckel diverticulum
144
What is the most common congenital anomaly of the GI tract? What percent of births does this occur in?
- meckel diverticulum
| - 2%
145
What are the rule of twos for Meckel diverticulum? (4)
- 2% of the population
- 2 inches long
- Located within 2 feet of the ileocecal valve
- Presents within 2 years of life
146
What are the complications with meckel diverticulum? (3)
- Bleeding
- Volvulus
- Intussusception
147
True or false: The majority of cases of Meckel diverticulum are symptomatic
false-- most are asymptomatic
148
What is a volvulus?
twisting of bowel along its mesentery, resulting in an obstruction and infarction
149
What is the most common location of a volvulus?
- Sigmoid colon (elderly)
| - Cecum (young)
150
What are the stools that occur with intussusception?
"Currant Jelly" stools
151
What is a "leading edge" in intussusception?
An outpouching of the wall of the intestines that acts for the proximal part of the bowel to hang onto, and pull
152
What is the most common cause of a leading edge in infants? Adults?
- Infants = lymphoid hyperplasia
| - Adults = Tumor
153
Why is the small bowel particularly susceptible to ischemic injury?
Uses a ton of ATP for transport of nutrients across the mucosa
154
What type of infarction can occur with embolism/thrombosis of the SMA or mesenteric veins?
Transmural
155
What is the mechanism by which infarctions of only the mucosa of the intestines occur?
Marked hypotension
156
What are the three clinical features of small bowel ischemia/infarction?
- Abdominal pain
- Bloody diarrhea
- Decreased bowel sounds
157
What is the pathophysiology celiac disease? What is the most pathogenic component of wheat?
- Immune mediated damage of the small bowel due to gluten exposure
- Gliadin
158
What are the gene loci that are associated with Celiac disease?
HLA DQ2 and DQ8
159
What are the three monosaccharides that are absorbed by the small intestines?
- Fructose
- Glucose
- Galactose
160
What is the enzyme that deamidates gliadin? What happens immunologically when this occurs?
- tTG (tissue transglutaminase)
| - Deamidated gliadin is presented by APCs and MHC II
161
What immune cells are involved in Celiac disease and mediate the tissue damage?
Helper T cells
162
What is dermatitis herpetiformis seen in Celiac disease? Treatment / prognosis for this?
- IgA deposition at the tips of the dermal papillae, causing herpes-like blisters in the skin
- This resolves with a gluten-free diet
163
What are the three IgA antibodies that can occur with Celiac disease?
1. Endomysium
2. tTG
3. Gliadin
164
What antibody subclass is used for celiac diagnosis if the pt does not produce IgA?
IgG
165
What are the three histological findings of Celiac disease?
- Flattening of the villi
- Hyperplasia of the crypts
- Increased intraepithelial lymphocytes
166
Which part of the small intestines is most affected by Celiac disease?
Duodenum
167
What two malignancies should you think of if a pt with Celiac disease presents with similar symptoms, despite good dietary control?
Small bowel carcinoma and T cell lymphoma
168
What is the pathophysiology of tropical sprue? When does it classically present?
Small bowel villi destruction by an unknown organism, after treatment for infectious diarrhea with Abx
169
What part(s) of the intestines are most affected by tropical sprue? What nutritional deficiencies can occur because of this?
- Jejunum and ileum
| - Folate and B12 deficiency, since these are absorbed here
170
What is the difference of location of intestinal changes between Celiac disease and tropical sprue?
```
celiac = duodenum
Tropical = jejunum and ileum
```
171
What is the causative agent of Whipple's disease?
Tropheryma Whippelii
172
Where does Tropheryma Whippelii reside in the body (which cells/ which layer)?
Within macrophages along the lamina propria of the small bowel
173
What causes the fat malabsorption with Whipple's disease?
Compression of lacteals by macrophages involved in inflammatory response
174
What are the s/sx of Whipple's disease? Why?
Steatorrhea / fat malabsorption d/t accumulation of organisms within the lamina propria of the intestines
175
Where do chylomicrons that are synthesized in the intestinal enterocytes go when absorbed? How does this release to the steatorrhea in Whipple's disease?
- Lamina propria to Lacteals to lymphatics.
| - Deposition of diseases macrophages will clog this up
176
What is the histological appearance of the macrophages in the lamina propria in whipple's disease? What is the stain that can be used to highlight these?
Foamy macrophages that are highlighted by PAS staining
177
What are the four places that Whipple's disease affects besides the GI tract?
- Synovium of the joints
- Cardiac valves
- Lymph nodes
- CNS
178
What is abetalipoproteinemia, and how is it inherited? What does this cause?
AR deficiency of -apoB48 and apoB100
| -fat malabsorption and absent LDL
179
What is the function of apoB48? B100?
- B48 = structural protein of the chylomicron
| - B100 = structural protein of VLDL and LDL
180
What are carcinoid tumors?
malignant proliferations of neuroendocrine cells, causing a low grade malignancy
181
What is the worst type of neuroendocrine tumor?
Small lung cell carcinoma
182
What is the immunohistological stain that is used to identify carcinoid tumors?
Chromogranin
183
What is Chromogranin?
Stain used to identify Carcinoid tumors
184
What is the most common site for the development of carcinoid tumors in the GI tract? What does this appear as?
Small bowel--grows as a submucosal polyp-like nodule
185
What is the chemical that Carcinoid tumors secrete? What is the lab test for this?
- 5HT
| - 5-HIAA (metabolite of 5HT) will be found in the urine
186
What happens when carcinoid tumors metastasize to the liver?
Are now able to dump 5HT directly into the portal vein, without being processed by the liver first
187
What is the cause of carcinoid heart disease?
Liver mets of carcinoid tumors dump 5HT directly into hepatic vein/IVC, causing fibrosis of the right heart, leading to tricuspid regurg and valvular stenosis
188
What are the three symptoms of 5HT overproduction by carcinoid tumors? What can trigger these?
- Bronchospasm
- Diarrhea
- Flushing
- EtOH or emotional distress
189
Why is it that carcinoid tumors that met to the liver cause only left sided valvular stenosis and tricuspid regurg, and NOT right sided problem?
Lungs have MAO, which will metabolize the excess 5HT
190
---What is the metabolite of 5HT that is made by MAO, and secreted in the urine?----
----5-HIAA----
191
What are the two major causes of acute appendicitis? Which is more common to children? Adults?
Obstruction via lymphoid hyperplasia (children) or fecaliths (adults)
192
What are the s/sx of a ruptured appendix?
Peritonitis that presents with guarding and rebound tenderness
193
What are the three classical characteristics of IBD?
Young jewish female with recurrent bloody diarrhea and abdominal pain
194
What parts of the GI wall are involved in ulcerative colitis?
Mucosal and submucosal (not muscularis or serosa)
195
What parts of the GI wall are involved in Crohn's disease?
Transmural (all parts of the wall)
196
Where does ulcerative colitis usually begin? What is the most proximal place it can involve?
- Rectum, works its way up
| - Cecum is the most proximal it can go
197
Which is contiguous, and which has skip lesions: ulcerative colitis, Crohn's disease
ulcerative colitis is contiguous
| Crohn's disease has skip lesions
198
Crypt abscesses are found in what disease (histologic hallmark)?
Ulcerative colitis (PMNs in crypts)
199
What is the gross appearance of ulcerative colitis?
Pseudopolyps and loss of haustra
200
What are the complications of ulcerative colitis?
toxic megacolon and carcinoma
201
What is the disease that is classically associated with ulcerative colitis?
Primary sclerosing cholangitis
202
What is the effect of smoking on ulcerative colitis? Crohn's disease?
```
UC = protects against
CD= increases risk
```
203
What are the two factors that are used to predict the risk of developing carcinoma from ulcerative colitis?
Extent of colonic involvement
| Duration of the disease
204
What is the antibody that is found in ulcerative colitis?
pANCA
205
What parts of the GI tract can Crohn's disease affect? What is the least common site?
- Mouth to anus
| - Rectum is the least common site
206
What are the usual symptoms of CD?
RLQ pain with non-bloody diarrhea
207
What is the inflammation seen in UC? CD?
```
UC = crypt abscesses
CD = Granulomas
```
208
What is the gross appearance of CD?
Cobblestone mucosa
209
What are the complications with CD?
Malabsorption
| fistula formation
210
What causes the contractions, stenosis, and the "creeping fat" of the GI tract with CD?
Fibroblasts in the granulomas cause fibrosis and contraction
211
What is the "string sign" suggestive of?
CD
212
What extra-GI disease is CD associated with?
Ankylosing spondylitis
213
Why are kidney stones more common with CD?
Increased ability for CaCO3 to be absorbed into the blood
214
"lead pipe appearance" on x-ray is suggestive of which IBD? What causes this?
Ulcerative colitis d/t loss of haustra
215
Why is it that the emesis is non-bilious with pyloric stenosis?
Gastric contents have not yet entered the intestines
216
How can chemotherapy cause stomach ulcers?
Decrease cell turnover in the stomach lining
217
What are the two ways of acquiring lactose intolerance?
- Loss of enzymes physiologically
| - Temporary loss of enzyme from a GI infection
