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BLOCK POSTING 2 > GIT PATHOLOGY > Flashcards

GIT PATHOLOGY Flashcards

1
Q

What is atresia in the GI tract?

A

Incomplete development of the GI tract commonly occurring at the esophagus near the tracheal bifurcation.

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2
Q

What is the clinical consequence of esophageal atresia?

A

It can lead to aspiration suffocation

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3
Q

What is the most common form of congenital intestinal atresia?

A

Imperforate anus due to failure of the cloacal diaphragm to involute.

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4
Q

What is stenosis in the GI tract?

A

A partial obstruction due to fibrous thickening of the wall commonly affecting the esophagus or small intestine.

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5
Q

What is a diaphragmatic hernia?

A

An incomplete formation of the diaphragm allowing abdominal viscera to herniate into the thoracic cavity.

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6
Q

What is an omphalocele?

A

Herniation of abdominal viscera into a ventral membranous sac due to incomplete closure of abdominal musculature.

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7
Q

How is gastroschisis different from omphalocele?

A

Gastroschisis involves herniation through all layers of the abdominal wall from peritoneum to skin.

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8
Q

What is ectopia in the GI tract?

A

Developmental rests of tissue in abnormal locations such as gastric mucosa in the esophagus (“inlet patch”).

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9
Q

What are complications of ectopic gastric mucosa in the esophagus?

A

Dysphagia esophagitis

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10
Q

What is gastric heterotopia?

A

Ectopic gastric mucosa in the small bowel or colon which may cause occult bleeding and peptic ulceration.

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11
Q

What is Meckel diverticulum?

A

A true diverticulum in the ileum caused by failure of the vitelline duct to involute.

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12
Q

What is the “rule of 2s” in Meckel diverticulum?

A

Occurs in 2% of the population within 2 feet of the ileocecal valve

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13
Q

What are symptoms of Meckel diverticulum?

A

Ectopic tissue may cause peptic ulceration occult bleeding

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14
Q

What is Hirschsprung disease?

A

Congenital aganglionic megacolon caused by failed migration or early death of neural crest cells leading to absence of ganglion cells in affected segments.

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15
Q

What are the clinical consequences of Hirschsprung disease?

A

Functional obstruction proximal dilation

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16
Q

What is required to diagnose Hirschsprung disease?

A

Biopsy showing absence of ganglion cells in affected segments.

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17
Q

What is Barrett esophagus?

A

A complication of chronic GERD characterized by intestinal metaplasia in esophageal squamous mucosa.

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18
Q

What is the risk associated with Barrett esophagus?

A

Increased risk of esophageal adenocarcinoma.

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19
Q

How is Barrett esophagus recognized endoscopically?

A

Tongues or patches of red velvety mucosa extending from the gastroesophageal junction.

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20
Q

What are the histological features of Barrett esophagus?

A

Presence of goblet cells in the metaplastic columnar epithelium.

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21
Q

How is Barrett esophagus diagnosed?

A

Endoscopy and biopsy prompted by GERD symptoms.

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22
Q

What is the most common associated defect with omphalocele?

A

40% of infants with omphalocele have other birth defects.

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23
Q

What complications can arise from ectopic pancreatic tissue in the pylorus?

A

Obstruction due to inflammation and scarring.

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24
Q

What are common associated conditions with esophageal atresia?

A

Congenital heart defects genitourinary malformations

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25
Q

What is the most common site for intestinal atresia?

A

The duodenum.

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26
Q

What is a key clinical feature of imperforate anus?

A

Failure of meconium passage in a newborn.

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27
Q

What causes stenosis in acquired forms?

A

Inflammatory scarring commonly affecting the esophagus or small intestine.

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28
Q

What is a tracheoesophageal fistula?

A

A congenital defect creating a connection between the esophagus and trachea.

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29
Q

What is the most common type of tracheoesophageal fistula?

A

Proximal esophageal atresia with the distal esophagus connected to the trachea.

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30
Q

What are clinical features of tracheoesophageal fistula?

A

Vomiting, polyhydramnios, abdominal distension, and aspiration.

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31
Q

What is an esophageal web?

A

A thin protrusion of esophageal mucosa, most often in the upper esophagus.

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32
Q

What are symptoms of esophageal web?

A

Dysphagia for poorly chewed food.

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33
Q

What syndrome is associated with esophageal web?

A

Plummer-Vinson syndrome (esophageal web, iron deficiency anemia, atrophic glossitis).

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34
Q

What is Zenker diverticulum?

A

An outpouching of pharyngeal mucosa through a defect in the muscular wall (false diverticulum).

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35
Q

Where does Zenker diverticulum occur?

A

Above the upper esophageal sphincter at the junction of the esophagus and pharynx.

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36
Q

What are clinical features of Zenker diverticulum?

A

Dysphagia, obstruction, and halitosis (bad breath).

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37
Q

What is Mallory-Weiss syndrome?

A

Longitudinal lacerations at the gastroesophageal junction caused by severe vomiting.

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38
Q

What are symptoms of Mallory-Weiss syndrome?

A

Painful hematemesis.

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39
Q

What is Boerhaave syndrome?

A

Esophageal rupture leading to air in the mediastinum and subcutaneous emphysema, often secondary to Mallory-Weiss syndrome.

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40
Q

What are esophageal varices?

A

Dilated submucosal veins in the lower esophagus, secondary to portal hypertension.

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41
Q

What is the clinical presentation of ruptured esophageal varices?

A

Painless hematemesis, commonly seen in cirrhosis patients.

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42
Q

What is achalasia?

A

Disordered esophageal motility with an inability to relax the lower esophageal sphincter (LES).

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43
Q

What causes achalasia?

A

Damage to ganglion cells in the myenteric plexus, either idiopathic or secondary (e.g., Chagas disease).

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44
Q

What are clinical features of achalasia?

A

Dysphagia for solids and liquids, putrid breath, high LES pressure, bird-beak sign on barium swallow, and risk for squamous cell carcinoma.

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45
Q

What is GERD?

A

Gastroesophageal reflux disease caused by reduced LES tone leading to acid reflux.

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46
Q

What are risk factors for GERD?

A

Alcohol, tobacco, obesity, fat-rich diet, caffeine, and hiatal hernia.

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47
Q

What are clinical features of GERD?

A

Heartburn, adult-onset asthma, cough, dental enamel damage, and complications like strictures or Barrett esophagus.

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48
Q

What is Barrett esophagus?

A

Metaplasia of the lower esophageal mucosa to nonciliated columnar epithelium with goblet cells.

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49
Q

What causes Barrett esophagus?

A

Chronic acidic stress from GERD.

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50
Q

What are complications of Barrett esophagus?

A

Progression to dysplasia and adenocarcinoma.

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51
Q

What is esophageal adenocarcinoma?

A

A malignant proliferation of glands, usually arising from Barrett esophagus in the lower third of the esophagus.

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52
Q

What is esophageal squamous cell carcinoma?

A

A malignant proliferation of squamous cells, usually in the upper or middle esophagus.

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53
Q

What are risk factors for esophageal squamous cell carcinoma?

A

Alcohol, tobacco, very hot tea, achalasia, Plummer-Vinson syndrome, and esophageal injury.

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54
Q

What are clinical features of esophageal carcinoma?

A

Progressive dysphagia (solids to liquids), weight loss, pain, hematemesis, and possibly hoarseness or cough.

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55
Q

Where does esophageal carcinoma metastasize based on location?

A

Upper third: cervical nodes; middle third: mediastinal or tracheobronchial nodes; lower third: celiac and gastric nodes.

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56
Q

What is the most common cause of chronic gastritis?

A

Infection with Helicobacter pylori.

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57
Q

What are other causes of chronic gastritis?

A

Autoimmune gastritis and chronic NSAID use.

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58
Q

What are the three main complications of chronic gastritis?

A

Peptic ulcer disease (PUD) mucosal atrophy with intestinal metaplasia

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59
Q

What type of gastritis is caused by H. pylori?

A

Antral gastritis with increased acid production.

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60
Q

What complications are associated with H. pylori gastritis?

A

Duodenal ulcers gastric ulcers

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61
Q

What are the four virulence factors of H. pylori?

A

Flagella (motility)
urease (elevates local pH)

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62
Q

What histological findings are seen in H. pylori gastritis?

A

Neutrophils in the lamina propria and gastric pits (forming pit abscesses) lymphoid aggregates (MALT)

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63
Q

What is the role of intestinal metaplasia in chronic gastritis?

A

Associated with goblet cells and columnar epithelium; increases the risk for gastric adenocarcinoma.

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64
Q

What is autoimmune gastritis?

A

A form of chronic gastritis caused by autoantibodies against parietal cells and intrinsic factor.

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65
Q

What is the hallmark feature of autoimmune gastritis?

A

Diffuse oxyntic mucosal damage in the gastric body and fundus.

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66
Q

What are the clinical consequences of autoimmune gastritis?

A

Hypochlorhydria or achlorhydria hypergastrinemia

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67
Q

What are the histological findings in autoimmune gastritis?

A

Loss of parietal and chief cells lymphoplasmacytic infiltration centered on gastric glands

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68
Q

What differentiates H. pylori gastritis from autoimmune gastritis?

A

H. pylori typically affects the antrum and spares the fundus while autoimmune gastritis targets the fundus and body but spares the antrum.

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69
Q

What is peptic ulcer disease (PUD)?

A

A condition characterized by acid-induced mucosal injury most often caused by H. pylori

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70
Q

What is gastroschisis?

A

A congenital malformation where the anterior abdominal wall fails to form exposing abdominal contents.

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71
Q

What is omphalocele?

A

Persistent herniation of bowel into the umbilical cord covered by peritoneum and amnion.

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72
Q

What is pyloric stenosis?

A

Congenital hypertrophy of the pyloric smooth muscle leading to obstruction.

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73
Q

How does pyloric stenosis present?

A

Projectile nonbilious vomiting visible peristalsis

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74
Q

What is the treatment for pyloric stenosis?

A

Myotomy (surgical correction).

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75
Q

What is acute gastritis?

A

Acidic damage to the stomach mucosa due to an imbalance between protective defenses and the acidic environment.

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76
Q

What are risk factors for acute gastritis?

A

Severe burns (Curling ulcer) NSAIDs

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77
Q

What are the possible outcomes of acid damage in acute gastritis?

A

Superficial inflammation erosion (loss of epithelium)

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78
Q

What are the two types of chronic gastritis?

A

Chronic autoimmune gastritis and chronic H. pylori gastritis.

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79
Q

What is the cause of chronic autoimmune gastritis?

A

Autoimmune destruction of parietal cells in the stomach body and fundus via T-cell mediated damage (type IV hypersensitivity).

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80
Q

What are the clinical features of autoimmune gastritis?

A

Achlorhydria hypergastrinemia

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81
Q

What is the most common cause of chronic gastritis?

A

Infection with Helicobacter pylori (90% of cases).

82
Q

How does H. pylori gastritis affect the stomach?

A

It weakens mucosal defenses primarily affecting the antrum

83
Q

What are the virulence factors of H. pylori?

A

Flagella urease (elevates pH)

84
Q

What is peptic ulcer disease (PUD)?

A

Solitary mucosal ulcer typically in the proximal duodenum (90%) or distal stomach (10%).

85
Q

What causes duodenal ulcers?

A

H. pylori infection (>95%) or Zollinger-Ellison syndrome (gastrin-secreting tumor).

86
Q

How does a duodenal ulcer present?

A

Epigastric pain that improves with meals.

87
Q

What are complications of duodenal ulcers?

A

Rupture causing bleeding from the gastroduodenal artery or acute pancreatitis.

88
Q

What causes gastric ulcers?

A

H. pylori (75%) NSAIDs

89
Q

How does a gastric ulcer present?

A

Epigastric pain that worsens with meals.

90
Q

What are complications of gastric ulcer rupture?

A

Bleeding from the left gastric artery.

91
Q

What is the differential diagnosis for ulcers?

A

Duodenal ulcers are rarely malignant but gastric ulcers may be due to intestinal-type gastric carcinoma.

92
Q

What is the morphology of benign ulcers?

A

Small (<3 cm) sharply demarcated (“punched-out”)

93
Q

What is the morphology of malignant ulcers?

A

Large irregular

94
Q

What is gastric carcinoma?

A

A malignant proliferation of gastric surface epithelial cells (adenocarcinoma).

95
Q

What are the two types of gastric carcinoma?

A

Intestinal type and diffuse type.

96
Q

What are the features of intestinal-type gastric carcinoma?

A

Associated with H. pylori intestinal metaplasia

97
Q

What are the features of diffuse-type gastric carcinoma?

A

Characterized by signet ring cells desmoplasia (linitis plastica)

98
Q

What are clinical features of gastric carcinoma?

A

Weight loss abdominal pain

99
Q

What are common sites of metastasis for gastric carcinoma?

A

Liver left supraclavicular node (Virchow node)

100
Q

Front

A

Back

101
Q

What percentage of gastric polyps do gastric adenomas represent?

A

Up to 10% of all gastric polyps.

102
Q

What is the typical age range for patients with gastric adenomas?

A

Between 50 and 60 years of age.

103
Q

Which gender is more commonly affected by gastric adenomas?

A

Males are affected three times more often than females.

104
Q

What background conditions are gastric adenomas almost always associated with?

A

Chronic gastritis with atrophy and intestinal metaplasia.

105
Q

What type of dysplasia is present in all gastrointestinal adenomas?

A

Epithelial dysplasia (low-grade or high-grade).

106
Q

What size of gastric adenoma lesion has an elevated risk of adenocarcinoma development?

A

Lesions greater than 2 cm in diameter.

107
Q

What percentage of gastric cancers are adenocarcinomas?

A

More than 90%.

108
Q

What are the early symptoms of gastric adenocarcinoma?

A

Dyspepsia, dysphagia, and nausea.

109
Q

Where is gastric carcinoma most commonly located?

A

In the antrum.

110
Q

What is the most common site for gastric carcinoma in pernicious anemia?

A

The fundus.

111
Q

What gene is strongly associated with familial gastric cancer?

A

The CDH1 gene, encoding E-cadherin.

112
Q

What is the key step in the development of sporadic diffuse gastric cancer?

A

Loss of E-cadherin.

113
Q

Which mutation increases the risk of diffuse gastric cancer?

A

BRCA2 mutations.

114
Q

What pathway is associated with sporadic intestinal-type gastric cancers?

A

The Wnt signaling pathway.

115
Q

What does the Lauren classification separate gastric cancers into?

A

Intestinal and diffuse types.

116
Q

Describe the morphology of intestinal-type gastric cancers.

A

Bulky, glandular structures forming exophytic masses or ulcerated tumors.

117
Q

What is the appearance of diffuse gastric cancer?

A

Infiltrative growth with signet ring cells, desmoplastic reaction, and a ‘leather bottle’ appearance (linitis plastica).

118
Q

Name the metastatic sites of gastric cancers.

A

Virchow’s node, Sister Mary Joseph node, Irish node, Krukenberg tumor, Blumer shelf.

119
Q

What accounts for 5% of gastric malignancies?

A

Primary lymphoma, mostly non-Hodgkin’s lymphoma.

120
Q

What is MALToma?

A

A mucosa-associated lymphoid tissue lymphoma involving NF-kB activation.

121
Q

Which tumor arises from intestinal cells of Cajal?

A

Gastrointestinal stromal tumor (GIST).

122
Q

What is volvulus?

A

Twisting of a bowel loop about its mesenteric attachment, leading to luminal and vascular compromise.

123
Q

What is intussusception?

A

Telescoping of a segment of bowel into the distal segment via peristalsis, common in children under 2 years.

124
Q

Name the key bacterial causes of infectious enterocolitis.

A

Cholera, Shigellosis, Campylobacter, Salmonella.

125
Q

What is inflammatory bowel disease (IBD)?

A

A chronic condition caused by inappropriate mucosal immune activation in genetically predisposed individuals.

126
Q

What are the two entities of IBD?

A

Crohn’s disease and ulcerative colitis.

127
Q

What factors contribute to IBD pathogenesis?

A

Host-GI flora interaction, epithelial dysfunction, aberrant mucosal immunity.

128
Q

Which immune signals contribute to IBD pathogenesis?

A

TNF, interferon-γ, IL-13, IL-10, TGF-β.

129
Q

Where does Crohn’s disease most commonly present?

A

Terminal ileum, ileocecal valve, and cecum.

130
Q

What is the characteristic appearance of Crohn’s disease mucosa?

A

Cobblestone appearance with skip lesions and elongated ulcers.

131
Q

What is ‘creeping fat’ in Crohn’s disease?

A

Mesenteric fat extending around the serosal surface of the bowel.

132
Q

Front

A

Back

133
Q

What characterizes the continuity of ulcerative colitis (UC)?

A

UC is a disease of continuity with no skip lesions.

134
Q

Which part of the GI tract does UC always involve?

A

The rectum, extending proximally in retrograde fashion.

135
Q

What is the term for UC limited to the rectum or rectosigmoid?

A

Ulcerative proctitis or ulcerative proctosigmoiditis.

136
Q

What is backwash ileitis?

A

Inflammation of the distal ileum in UC.

137
Q

How do ulcers in UC align?

A

Ulcers are aligned along the long axis of the colon but do not replicate Crohn disease’s serpentine ulcers.

138
Q

What are pseudopolyps in UC?

A

Isolated islands of regenerating mucosa bulging into the lumen, creating small elevations.

139
Q

What distinguishes microscopic inflammation in UC?

A

It is generally limited to the mucosa with crypt abscesses, ulceration, and chronic mucosal damage but lacks fissures, aphthous ulcers, or granulomas.

140
Q

What is the most common malignancy of the GI tract?

A

Adenocarcinoma of the colon.

141
Q

What is the global annual incidence of colon adenocarcinoma?

A

1.2 million cases per year.

142
Q

Which regions have the highest incidence of colon adenocarcinoma?

A

Australia, New Zealand, Japan, North & Western Europe.

143
Q

What genetic syndromes are associated with colon adenocarcinoma risk?

A

HNPCC (Lynch syndrome), FAP (APC mutation), Peutz-Jeghers, Juvenile polyposis syndrome, PTEN hamartoma syndrome, Birt-Hogg-Dube syndrome.

144
Q

What non-genetic factors increase the risk of colon adenocarcinoma?

A

Diet, alcohol, smoking, IBD, infections, iatrogenic factors.

145
Q

What is the adenoma-carcinoma sequence?

A

A multihit genetic mechanism involving the APC/β-catenin pathway associated with Wnt signaling.

146
Q

What happens when APC is lost in the adenoma-carcinoma sequence?

A

β-catenin accumulates, translocates to the nucleus, and activates genes promoting proliferation.

147
Q

What is microsatellite instability (MSI)?

A

A condition where mutations accumulate in microsatellite repeats due to DNA mismatch repair deficiency.

148
Q

How does TGF-β mutation contribute to colon cancer?

A

Loss of TGF-β receptor type II prevents inhibition of colonic epithelial cell proliferation.

149
Q

What are the gross morphologies of colon tumors in the right vs. distal colon?

A

Polypoid, exophytic masses in the cecum/right colon; annular ‘napkin-ring’ masses in the distal colon.

150
Q

What is the microscopic morphology of adenocarcinoma in the colon?

A

Composed of tall, columnar cells resembling adenomatous neoplastic epithelium with invasion into deeper layers.

151
Q

What are less common histological features of colon adenocarcinoma?

A

Neuroendocrine differentiation, signet-ring features, squamous differentiation, and strong desmoplastic responses.

152
Q

Front

A

Back

153
Q

What is duodenal atresia?

A

Congenital failure of the duodenum to canalize; associated with Down syndrome.

154
Q

What are the clinical features of duodenal atresia?

A

Polyhydramnios, distension of stomach and blind loop (‘double bubble’), bilious vomiting.

155
Q

What is Meckel diverticulum?

A

Outpouching of all three layers of the bowel wall (true diverticulum).

156
Q

What causes Meckel diverticulum?

A

Failure of the vitelline duct to involute.

157
Q

What is the ‘Rule of 2s’ in Meckel diverticulum?

A

Seen in 2% of the population, 2 inches long, located within 2 feet of the ileocecal valve.

158
Q

What is volvulus?

A

Twisting of bowel along its mesentery causing obstruction and ischemia.

159
Q

What are common locations for volvulus?

A

Sigmoid colon (elderly) and cecum (young adults).

160
Q

What is intussusception?

A

Telescoping of a proximal bowel segment into a distal segment, causing obstruction and ischemia.

161
Q

What causes intussusception in children vs. adults?

A

Children: lymphoid hyperplasia (e.g., rotavirus). Adults: tumor.

162
Q

What causes transmural small bowel infarction?

A

Thrombosis/embolism of the superior mesenteric artery or thrombosis of the mesenteric vein.

163
Q

What causes mucosal small bowel infarction?

A

Marked hypotension.

164
Q

What are the clinical features of small bowel infarction?

A

Abdominal pain, bloody diarrhea, and decreased bowel sounds.

165
Q

What causes lactose intolerance?

A

Decreased function of lactase enzyme in the brush border of enterocytes.

166
Q

What are the clinical features of lactose intolerance?

A

Abdominal distension and diarrhea after consuming milk products.

167
Q

What is celiac disease?

A

Immune-mediated damage to small bowel villi due to gluten exposure; associated with HLA-DQ2 and DQ8.

168
Q

What are the late complications of untreated celiac disease?

A

Small bowel carcinoma and T-cell lymphoma.

169
Q

What is tropical sprue?

A

Damage to small bowel villi in tropical regions after infectious diarrhea; responds to antibiotics.

170
Q

What is Whipple disease?

A

Systemic tissue damage by Tropheryma whippelii, involving macrophages in the lamina propria.

171
Q

What is abetalipoproteinemia?

A

Autosomal recessive deficiency of apolipoproteins B-48 and B-100, causing malabsorption and absent plasma VLDL and LDL.

172
Q

What is a carcinoid tumor?

A

Malignant proliferation of neuroendocrine cells; often secretes serotonin.

173
Q

What are the clinical features of carcinoid syndrome?

A

Bronchospasm, diarrhea, flushing of the skin; triggered by alcohol or stress.

174
Q

What is acute appendicitis?

A

Acute inflammation of the appendix caused by obstruction (lymphoid hyperplasia in children, fecalith in adults).

175
Q

What are the clinical features of acute appendicitis?

A

Periumbilical pain localizing to RLQ (McBurney point), fever, nausea.

176
Q

What is Hirschsprung disease?

A

Congenital failure of ganglion cells to migrate into the myenteric and submucosal plexus, causing obstruction.

177
Q

What are colonic diverticula?

A

Outpouchings of mucosa and submucosa through the muscularis propria; associated with constipation and low-fiber diets.

178
Q

What is angiodysplasia?

A

Acquired malformation of mucosal and submucosal capillary beds, causing hematochezia in older adults.

179
Q

What is ischemic colitis?

A

Ischemic damage to the colon, usually at the splenic flexure; commonly caused by atherosclerosis of the SMA.

180
Q

What is familial adenomatous polyposis (FAP)?

A

Autosomal dominant disorder with 100s-1000s of adenomatous colonic polyps due to APC mutation.

181
Q

What is Peutz-Jeghers syndrome?

A

Hamartomatous polyps throughout the GI tract and mucocutaneous hyperpigmentation; increased risk of GI and other cancers.

182
Q

What is colorectal carcinoma?

A

Carcinoma of colonic/rectal mucosa; the third most common cancer worldwide.

183
Q

What are left-sided vs. right-sided presentations of colorectal carcinoma?

A

Left-sided: napkin-ring lesion, LLQ pain, blood-streaked stool. Right-sided: raised lesion, iron-deficiency anemia, vague pain.

184
Q

Front

A

Back

185
Q

What part of the wall is involved in ulcerative colitis (UC)?

A

Mucosal and submucosal ulcers.

186
Q

What part of the wall is involved in Crohn’s disease?

A

Full-thickness inflammation with knife-like fissures.

187
Q

What is the location of UC?

A

Begins in the rectum and can extend proximally up to the cecum; continuous involvement; remainder of GI tract unaffected.

188
Q

What is the location of Crohn’s disease?

A

Anywhere from mouth to anus with skip lesions; terminal ileum is the most common site, rectum is the least common.

189
Q

What are the symptoms of UC?

A

Left lower quadrant pain (rectum) with bloody diarrhea.

190
Q

What are the symptoms of Crohn’s disease?

A

Right lower quadrant pain (ileum) with non-bloody diarrhea.

191
Q

What microscopic findings are seen in UC?

A

Crypt abscesses with neutrophils.

192
Q

What microscopic findings are seen in Crohn’s disease?

A

Lymphoid aggregates with granulomas (40% of cases).

193
Q

What is the gross appearance of UC?

A

Pseudopolyps and loss of haustra (‘lead pipe’ sign on imaging).

194
Q

What is the gross appearance of Crohn’s disease?

A

Cobblestone mucosa, creeping fat, and strictures (‘string sign’ on imaging).

195
Q

What are the complications of UC?

A

Toxic megacolon and carcinoma (risk increases with extent and duration of disease; generally after >10 years).

196
Q

What are the complications of Crohn’s disease?

A

Malabsorption with nutritional deficiencies, calcium oxalate nephrolithiasis, fistula formation, and carcinoma if colonic disease is present.

197
Q

What diseases are associated with UC?

A

Primary sclerosing cholangitis and p-ANCA positivity.

198
Q

What diseases are associated with Crohn’s disease?

A

Ankylosing spondylitis, sacroiliitis, migratory polyarthritis, erythema nodosum, and uveitis.

199
Q

How does smoking affect UC?

A

Protects against UC.

200
Q

How does smoking affect Crohn’s disease?

A

Increases the risk for Crohn’s disease.

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