Gi 8A

Front 1

Describe the radiographic appearance of achalasia.

Back 1

Dilation of esophagus with "bird beak" appearance

Front 2

Name four possible causes of 2° achalasia.

Back 2

Chagas dz; DM neuropathy; sarcoidosis; tumor compression

Front 3

Zenker's diverticulum is an example of a __ diverticulum. What does this signify?

Back 3

False diverticulum - outpouching only includes mucosa and submucosa (not muscularis externa)

Front 4

Where is Zenker's diverticulum typically located?

Back 4

Immediately above the upper esophageal sphincter

Front 5

Epiphrenic diverticulum is an example of a __ diverticulum. What does this signify?

Back 5

True diverticulum - outpouching of all layers, including muscularis externa

Front 6

Where is an epiphrenic diverticulum located?

Back 6

Just above the LES

Front 7

What is the difference between a pulsion diverticulum and a traction diverticulum? Give an example of each.

Back 7

Pulsion: high intraluminal pressure pushing against weak esophageal wall; ex. Zenker's diverticulum
Traction: pulling forces from outside the esophagus (e.g. mediastinal inflammation); ex. Epiphrenic diverticulum

Front 8

Esophageal varices are inevitably due to __. Give two causes of this condition.

Back 8

Portal HTN
Liver cirrhosis (2/2 EtOH or HCV), portal/hepatic vein thrombosis

Front 9

What are the symptoms of esophageal varices?

Back 9

Asymptomatic until rupture
After rupture: massive hematemesis

Front 10

What is the mortality of esophageal varices?

Back 10

40-50% per rupture event

Front 11

What is scleroderma? How does it manifest in the esophagus? (Name three.)

Back 11

Chronic autoimmune disease
- lumenal stenosis
- esophageal atrophy
- ulceration

Front 12

Viral esophagitis is most commonly seen in what group?

Back 12

Immunocompromised individuals

Front 13

Name three fungal infections which may affect the esophagus.

Back 13

Candida, Mucor, Aspergillus

Front 14

What is the MCC esophagitis?

Back 14

Reflux of GI content (GERD)

Front 15

What is the "classical" symptom of GERD?

Back 15

Substernal pain (heartburn) worse in the supine position

Front 16

Describe the pathogenesis of GERD.

Back 16

Incompetent LES and/or sliding hiatal hernia

Front 17

Give four risk factors for GERD.

Back 17

Obesity; EtOH; smoking; pregnancy

Front 18

Describe the micro appearance of an esophagus with GERD.

Back 18

Hyperplasia of basal epithelial layer
Increased height of papillae (blood supply)
Intraepithelial eosinophils
Intercellular edema

Front 19

Name two possible complications and one possible consequence of GERD.

Back 19

Complications: esophageal stricture or bleeding
Predisposes to: Barrett's esophagus

Front 20

GERD predisposes a patient to __.

Back 20

Barrett's esophagus → esophageal adenocarcinoma

Front 21

Eosinophilic esophagitis typically occurs in what group?

Back 21

Children

Front 22

Describe the clinical manifestations of eosinophilic esophagitis.

Back 22

Children: presents with GERD-like sx
Adults: presents with dysphagia

Front 23

Describe the micro appearance of eosinophilic esophagitis.

Back 23

Intraepithelial eosinophils (>25 per high power field)

Front 24

How can you tell eosinophilic esophagitis apart from GERD?

Back 24

EE is resistant to proton pump inhibitors

Front 25

Describe the micro appearance of Barrett's esophagus.

Back 25

Irregular Z-lines with "salmon colored tongues"
Goblet cell proliferation (intestinal metaplasia)

Front 26

How do you grade epithelial dysplasia in the esophagus?

Back 26

Low grade: polarity is maintained
High grade: polarity is lost, but no invasion
Indeterminate grade: inflamation
Intramucosal adenocarcinoma: invasion into lamina propria
Adenocarcinoma: invasion beyond lamina propria

Front 27

Give six examples of benign neoplasms in the esophagus.

Back 27

Fibromas, lipomas, fibrolipomas, leiomyomas, stromal tumors, granular cell tumors

Front 28

Give three epidemiologic factors associated with the development of squamous cell carcinoma of the esophagus.

Back 28

EtOH; smoking; black (African-American)

Front 29

What is the typical location of esophageal squamous cell carcinoma?

Back 29

Upper 2/3

Front 30

Describe the symptoms of esophageal squamous cell carcinoma.

Back 30

Progressive dysphagia; solids are more affected than liquids

Front 31

Describe the gross appearance of esophageal squamous cell carcinoma.

Back 31

Fungating, ulcerating lesion in proximal 2/3 of esophagus

Front 32

Describe the micro appearance of esophageal squamous cell carcinoma.

Back 32

Malignant squamous cells with eosinophilic cytoplasm

Front 33

Give two factors associated with the development of esophageal adenocarcinoma.

Back 33

White (Caucasian); Barrett's esophagus (usually 2/2 GERD)

Front 34

Epidemiologically, what group is at highest risk for esophageal squamous cell carcinoma? Esophageal adenocarcinoma?

Back 34

Black males
White males

Front 35

Describe the symptoms of esophageal adenocarcinoma.

Back 35

Progressive dysphagia; solids are more affected than liquids

Front 36

What is the typical location of esophageal adenocarcinoma?

Back 36

Lower 1/3

Front 37

Describe the micro appearance of esophageal adenocarcinoma.

Back 37

Malignant glandular cells with goblet cells and complex architecture

Front 38

Name five malignant tumors that may arise in the esophagus.

Back 38

Squamous cell carcinoma
Adenocarcinoma
Leiomyosarcoma
Neuroendocrine tumors (carcinoid)
Adenoid cystic adenocarcinoma

Front 39

What are the two general causes of odynophagia?

Back 39

HIV related infection; drugs (NSAIDs, Fe)

Front 40

Define dysphagia.

Back 40

Failure of transport

Front 41

Give three general causes of dysphagia.

Back 41

Failure of LES relaxation; physical obstruction; poor neuromuscular function

Front 42

Define transfer dysphagia. It is associated with what pathology?

Back 42

Failure to coordinate pharyngeal constriction and UES relaxation to permit bolus passage into esophagus. Associated with neuromuscular damage

Front 43

Which is affected first: solids or liquids?
- Transfer dysphagia
- Physical obstruction
- Organic obstruction

Back 43

- Liquid
- Solid
- Liquid

Front 44

Give two possible consequences of transfer dysphagia.

Back 44

Nasal regurgitation; aspiration

Front 45

Solid dysphagia is typically associated with __ obstruction. Give an example of this type of obstruction.

Back 45

Physical; tumor mass

Front 46

Intermittent solid dysphagia is associated with what pathology?

Back 46

Schatzki's ring

Front 47

Progressive solid dysphagia is associated with what pathology?

Back 47

Growing tumor

Front 48

Liquid dysphagia is typically associated with __ obstruction. Give an example of this type of obstruction.

Back 48

Organic; neuromuscular damage

Front 49

Define odynophagia. Give two common causes.

Back 49

Pain on swallowing; usually due to infection or drug-induced acute esophagitis

Front 50

Name five causes of odynophagia.

Back 50

Herpes infection; CMV infection; Candidiasis; NSAID-induced esophagitis; Fe-induced esophagitis

Front 51

Give four ways to differentiate odynophagia from cardiac chest pain.

Back 51

1. Odynophagia associated with eating
2. Odynophagia associated with dysphagia
3. Cardiac chest pain related to exercise
4. Odynophagia lasts longer than cardiac chest pain

Front 52

Give the classical description of heartburn.

Back 52

Lower substernal pain radiating to epigastrum or shoulders; worse when supine (in GERD)

Front 53

What is water brash? It is typically associated with what pathology?

Back 53

Sudden reflux of large volume of clear fluid in oropharynx
Associated with reflux esophagitis

Front 54

Give one non-GI manifestation of recurrent reflux.

Back 54

Chronic aspiration → pulmonary Sx

Front 55

Explain the pathogenesis of an acquired tracheoesophageal fistula.

Back 55

Tumor erodes between esophagus and tracheobronchial tree

Front 56

What are the symptoms of an acquired tracheoesophageal fistula?

Back 56

Coughing; choking with eating

Front 57

What is a Mallory-Weiss tear? Where does it occur?

Back 57

Painful mucosal lacerations at the GE junction

Front 58

Mallory Weiss tears are usually a result of __.

Back 58

Severe vomiting (alcoholics or bulemics)

Front 59

A patient with h/o bulemia presents to the ER c/o sudden hematemesis and pain. Dx.

Back 59

Mallory Weiss tear

Front 60

A patient with h/o heavy EtOH use presents to the ER c/o sudden hematemesis and pain. Dx.

Back 60

Mallory Weiss tear

Front 61

A patient with h/o heavy EtOH use presents to the ER c/o sudden hematemesis. He denies pain. Dx.

Back 61

Esophageal variceal bleeding

Front 62

Where do esophageal varices typically occur (both along the length of the esophagus and in what structure)?

Back 62

Distal 1/3 of esophagus; submucosal veins

Front 63

What does a barium swallow test?

Back 63

Gross transport (swallowing and esophageal transport)

Front 64

What does manometry test?

Back 64

Muscular coordination for peristalsis

Front 65

Endoscopy is most useful for elucidating what features? What is another advantage of endoscopy?

Back 65

Mucosal details and gross tumors; can take biopsy for cytology or Cx

Front 66

What does pH monitoring test for?

Back 66

Acid reflux

Front 67

What do nuclear medicine scans test for in the esophagus?

Back 67

Bolus transport

Front 68

What is the difference between a sliding and a paraesophageal hiatal hernia?

Back 68

Sliding: GE junction goes through the diaphragm
Paraesophageal: GE junction remains fixed beneath diaphragm; another part of stomach (usually fundus) protrudes into the mediastinum

Front 69

Paraesophageal hiatal hernia may lead to __.

Back 69

stomach strangulation

Front 70

What is Schatzki's ring? Where does it occur?

Back 70

Lower esophageal ring; occurs at squamocolumnar junction

Front 71

How might Schatzki's ring manifest?

Back 71

Slight narrowing of esophageal lumen → intermittent obstruction with large meal ingestion

Front 72

Name the three major kinds of esophageal diverticulum. Where does each occur?

Back 72

Zenker's: above UES (and above cricopharyngeus muscle)
Midesophageal: middle ~1/3 of esophagus
Epiphrenic: distal esophagus just above diaphragm/LES

Front 73

Give three symptoms of Zenker's diverticulum.

Back 73

Halitosis; dysphagia; obstruction

Front 74

Name five neuromuscular diseases of the esophagus.

Back 74

Achalasia; diffuse esophageal spasm; scleroderma; nutcracker esophagus; hypertensive LES

Front 75

Describe the pathogenesis of achalasia. What is a similar defect in the colon?

Back 75

Preganglionic defect → failure of peristalsis and LES relaxation
Similar to Hirschprung's dz in colon

Front 76

Give four clinical manifestations of achalasia.

Back 76

Worsening solid & liquid dysphagia over a period of months → years
Dull substernal pain
Regurgitation of undigested products
Halitosis

Front 77

What are two treatments of achalasia?

Back 77

Pneumatic LES dilation
Heller myotomy

Front 78

Describe the radiographic appearance of diffuse esophageal spasm.

Back 78

Corkscrew esophagus

Front 79

What is a diffuse esophageal spasm?

Back 79

Disordered, non-peristaltic contractions of esophagus

Front 80

What is the most commonly misdiagnosed primary GI disorder?

Back 80

Diffuse esophageal spasm

Front 81

What is the characteristic finding in scleroderma of the esophagus?

Back 81

Esophageal aperistalsis; weak LES

Front 82

Describe the radiographic appearance of an esophagus with scleroderma.

Back 82

Dilated, atonic esophagus

Front 83

Symptoms of esophageal scleroderma are due to what?

Back 83

Secondary reflux esophagitis

Front 84

What is "nutcracker esophagus"?

Back 84

High pressure, but normal peristaltic contraction

Front 85

What is a hypertensive LES?

Back 85

Elevated resting tone of LES

Front 86

What are the four major regions of the stomach?

Back 86

Cardia; fundus; body; antrum

Front 87

What four cell types are found in the fundus and body? What does each cell secrete?

Back 87

Parietal (HCl); chief (pepsinogen); ECL (histamine); D (somatostatin)

Front 88

What two regions of the stomach are indistinguishable histologically?

Back 88

Fundus and body

Front 89

How do you tell apart gastric cardia and gastric antrum?

Back 89

Depth of the pits: cardia pits are shallow, antrum pits are deep

Front 90

What causes congenital pyloric stenosis?

Back 90

Hypertrophy of the circular muscular layer of the pyloric sphincter

Front 91

Describe the SSx of congenital pyloric stenosis.

Back 91

Palpable abdominal mass
Episodic projectile vomiting within the first 2 weeks of life

Front 92

What is MCC acute gastritis?

Back 92

NSAIDs

Front 93

Describe the micro appearance of mild acute gastritis.

Back 93

Normal epithelium; edema; congestion; red and "angry looking"

Front 94

Describe the micro appearance of severe acute gastritis.

Back 94

Sloughing of epithelium; bleeding into lamina propria; acute inflammatory infiltrate (PMNs predominate)

Front 95

Describe the micro appearance of erosive acute gastritis.

Back 95

Complete loss of epithelium

Front 96

Describe the pathogenesis of acute gastritis.

Back 96

Injury to mucosal barrier → back-diffusion of H+

Front 97

Specifically describe the pathogenesis of acute gastritis due to ischemia.

Back 97

AV shunt, followed by reperfusion → ischemia → hemorrhage

Front 98

What are three non-GI complaints that may cause acute gastritis?

Back 98

Uremia; burns; brain injury

Front 99

What are four iatrogenic causes of acute gastritis?

Back 99

Radiation; chemotherapy; NG tube; NSAIDs

Front 100

What are two infectious causes of acute gastritis?

Back 100

H. pylori; GI viruses

Front 101

Burns may cause what kind of acute gastritis?

Back 101

Curling's ulcer

Front 102

Brain injury may cause what kind of acute gastritis?

Back 102

Cushing's ulcer

Front 103

What are five SSx of severe acute gastritis?

Back 103

Erosion; ulcer; bleeding; nausea; vomiting

Front 104

Compare chronic gastritis due to H. pylori with that due to autoimmune gastritis?

Back 104

H. pylori: hyperchlorhydria, high peptic ulcers, high MALT lymphomas; usually in antrum
Autoimmune: achlorhydria, mucosal atrophy; usually in body

Front 105

__ gene is highly associated with adenocarcinoma in H. pylori chronic gastritis.

Back 105

CagA

Front 106

CagA gene is associated with what two cancers in the GI tract? What is typically the cause?

Back 106

Adenocarcinoma and MALT lymphoma
Associated with H. pylori

Front 107

What is the MCC chronic gastritis?

Back 107

H. pylori gastritis

Front 108

How is H. pylori transmitted? Give four epidemiologic associations.

Back 108

Fecal-oral
Poverty; crowding; low education; non-White

Front 109

When does H. pylori infection usually occur? When does it present with Sx?

Back 109

Childhood; middle adulthood (long latency)

Front 110

What can be seen on micro exam of a stomach with chronic H. pylori gastritis?

Back 110

Gram negative rods on surface epithelial cells within mucus
PMNs in epithelium; PMNs, plasma cells, lymphocytes, and lymphoid follicles in lamina propria

Front 111

What immune cells may be seen in chronic H. pylori gastritis? Where is each cell located?

Back 111

PMNs (epithelium & lamina propria); plasma cells, lymphocytes, lymphoid follicles (lamina propria only)

Front 112

What is the cause of autoimmune gastritis?

Back 112

Ab against parietal cells (or possibly against intrinsic factor)

Front 113

What cancer(s) is/are seen in association with chronic H. pylori gastritis?

Back 113

Adenocarcinoma; MALT lymphoma

Front 114

What cancer(s) is/are seen in association with chronic autoimmune gastritis?

Back 114

Gastric carcinoid tumor

Front 115

Why does autoimmune gastritis have a correlation with gastric carcinoid tumor?

Back 115

Gastrin overproduction (due to destruction of parietal cells)

Front 116

What cells produce gastrin? In which region(s) of the stomach are these found?

Back 116

Neuroendocrine G cells; found in antrum

Front 117

What is the relative prognosis of 1° gastric carcinoid tumors compared with gastric carcinoid tumors 2/2 autoimmune gastritis?

Back 117

Better prognosis with autoimmune gastritis

Front 118

Give four SSx associated with autoimmune gastritis.

Back 118

Achlorhydria
Pernicious anemia (loss of GIF → vit B12 deficiency)
Autoimmune dz (thyroiditis, Addison's)
Hormonal dysregulation (gastrin ↑, pepsinogen ↓)

Front 119

Autoimmune gastritis primarily affects which region(s) of the stomach?

Back 119

Body & fundus (oxyntic mucosa)

Front 120

Describe the gross appearance of autoimmune gastritis.

Back 120

Mucosal atrophy; decreased or loss of rugal folds

Front 121

Describe the micro appearance of autoimmune gastritis.

Back 121

Chronic inflammatory infiltrates
Pseudoantral metaplasia (G cell and ECL cell hyperplasia)
Intestinal metaplasia

Front 122

Give two causes of reactive gastropathy.

Back 122

Chronic NSAID use; GI reflux

Front 123

What region is most affected by reactive gastropathy?

Back 123

Antrum

Front 124

Describe the micro appearance of reactive gastropathy.

Back 124

Damage without inflammation
- Epithelium: elongation & widening of foveolae; reactive cells
- Lamina propria: fibrosis; edema

Front 125

Give four possible complications of chronic gastritis.

Back 125

Peptic ulcer disease
Atrophy
Intestinal Metaplasia
Dysplasia

Front 126

Peptic ulcer disease is associated with what pathology?

Back 126

Chronic H. pylori gastritis with hyperchlorhydria

Front 127

PUD usually occurs where in the stomach?

Back 127

Proximal duodenum & lesser curvature of the stomach (antrum)

Front 128

What is the prognosis of PUD?

Back 128

Not a pre-cancerous lesion! Could progress to obstruction or perforation

Front 129

Name three possible complications of PUD.

Back 129

Upper GI bleeding → hematemesis/melena
Obstruction
Perforation

Front 130

Describe the micro appearance of peptic ulcer disease.

Back 130

Solitary lesions with a clean base

Front 131

An ulcer must extend at least as far as the __.

Back 131

muscularis mucosa

Front 132

What are the layers of the ulcer bed?

Back 132

Inflammatory exudate
Necrosis
Granulation tissue
Chronic inflammation
Fibrosis

Front 133

Gastric atrophy is typical of what pathologic process?

Back 133

Chronic gastritis of body and antrum

Front 134

Intestinal metaplasia is associated with what two conditions?

Back 134

Chronic H. pylori gastritis
Autoimmune gastritis

Front 135

Intestinal metaplasia may predispose to what?

Back 135

Dysplasia → malignancy

Front 136

Give five pathologic features of gastric dysplasia.

Back 136

Abnormal mitosis
Hyperchromasia
Pleomorphism
Nuclear elongation & stratification
Loss of polarity

Front 137

What is a sign of high grade gastric dysplasia?

Back 137

Loss of polarity

Front 138

What is the cause of Zollinger Ellison syndrome?

Back 138

Gastrinoma (gastrin-producing pancreatic islet cell tumor)

Front 139

How does Zollinger Ellison Syndrome create gastric problems?

Back 139

Gastrin → increased H+ production by parietal cells → multiple duodenal ulcers in aberrant sites
Also causes diarrhea via secretory, exudative, and osmotic processes

Front 140

Zollinger Ellison Sd is associated with what condition?

Back 140

Multiple endocrine neoplasia, type 1

Front 141

What three organs are typically affected in MEN1?

Back 141

Pancreas, parathyroid, pituitary

Front 142

What are two types of benign gastric neoplasms?

Back 142

Fundic polyps; hyperplastic polyps

Front 143

Fundic polyps cause what pathological anomaly?

Back 143

Dilated fundic glands

Front 144

Sporadic fundic polyps are typically due to __.

Back 144

PPI use

Front 145

What is the difference between fundic polyps due to PPI use vs. those due to FAP?

Back 145

PPI: sporadic, single benign polyps
FAP: multiple pre-cancerous polyps

Front 146

In which area of the stomach do hyperplastic polyps typically arise?

Back 146

Antrum

Front 147

Hyperplastic polyps are typically due to __.

Back 147

Chronic gastritis

Front 148

What is the MCC malignant epithelial tumor of the stomach?

Back 148

Gastric adenocarcinoma

Front 149

Give six possible causes of gastric adenocarcinoma.

Back 149

Smoked food; high salt intake; H. pylori; achlohydria (2/2 chronic gastritis); adenomatous polyps; villous polyps

Front 150

Give two symptoms and three signs of gastric adenocarcinoma.

Back 150

Sx: epigastric pain, dyspepsia (epigastric pain related to eating)
Signs: occult bleeding, anemia, weight loss

Front 151

Define dyspepsia.

Back 151

Recurrent epigastric pain; typically increases immediately after eating but decreases later on

Front 152

What is the metastatic potential of gastric adenocarcinoma?

Back 152

Aggressive! Spreads to adjacent organs and regional lymph nodes; distal spread is common

Front 153

Give three common sites of distal metastasis in gastric adenocarcinoma.

Back 153

Ovaries (Krukenberg tumors)
Left supraclavicular lymph node (Virchow's node)
Periumbilical region (Sister Mary Joseph SC nodule)

Front 154

What is the prognosis of gastric adenocarcinoma?

Back 154

Poor

Front 155

Gastric adenocarcinoma typically affects which area(s) of the stomach?

Back 155

Antrum; lesser curvature

Front 156

Which form of gastric adenocarcinoma is typically associated with H. pylori?

Back 156

Intestinal type

Front 157

Your patient presents with gastric adenocarcinoma, but an IgG for H. pylori is negative. Which type do you expect? What is the mutation?

Back 157

Diffuse type gastric adenocarcinoma
CDH1 mutation → absence of E-cadherins

Front 158

Your patient presents with gastric adenocarcinoma, and an IgG for H. pylori is positive. What type do you suspect? What is the likely mutation?

Back 158

Intestinal type
APC/beta-catenin mutation OR microsatellite instability

Front 159

Describe the gross appearance of an intestinal type gastric adenocarcinoma.

Back 159

Polyploid, fungating, bulky mass

Front 160

Describe the gross appearance of a diffuse type gastric adenocarcinoma.

Back 160

Linitis plastica (leather bottle) stomach with diffuse thickening and ulceration

Front 161

Describe the micro appearance of an intestinal type gastric adenocarcinoma.

Back 161

Well-differentiated glands

Front 162

Describe the micro appearance of a diffuse type gastric adenocarcinoma.

Back 162

Signet ring cells; poorly differentiated glands

Front 163

What is the MCC mesenchymal tumor of the GI tract?

Back 163

GI stromal tumor (GIST)

Front 164

From what cells does GIST arise? What cell surface markers are likely?

Back 164

Cells of Cajal; CD34 and c-KIT

Front 165

What is the mutation in GI stromal tumors?

Back 165

c-KIT is mutated → proliferation

Front 166

What are two possible treatments for GIST?

Back 166

Surgical resection; Gleevec

Front 167

Describe the gross appearance of a GI stromal tumor.

Back 167

Solitary, fleshy, well-circumscribed lesions

Front 168

Describe the micro appearance of a GI stromal tumor.

Back 168

Spindle or epithelioid-shaped cells which stain c-KIT positive

Front 169

The prognosis of GIST depends on three factors. Name them.

Back 169

Location: GIST in stomach is less aggressive than GIST in small intestine
Mitosis rate: high → more aggressive
Size: large → more aggressive

Front 170

What is the #1 site of metastasis for extranodal lymphoma?

Back 170

GI tract

Front 171

What are the two most common GI lymphomas?

Back 171

Marginal zone B cell lymphoma (MALToma)
Diffuse Large B cell Lymphoma

Front 172

What portion of the GI tract is commonly affected by MALToma?

Back 172

Stomach

Front 173

What is the difference between a "responsive" and a "non-responsive" MALToma?

Back 173

Responsive: eradicate H. pylori → goes away
Non-responsive: H. pylori treatment → nothing

Front 174

MALToma may transform into what other condition?

Back 174

Diffuse large B cell lymphoma

Front 175

What cell markers are typically seen in MALToma?

Back 175

CD19, CD20

Front 176

Describe the micro appearance of a MALToma.

Back 176

Lymphoid infiltrate; lympho-epithelial destruction

Front 177

What three diseases most commonly cause dyspepsia?

Back 177

Peptic ulcer disease
Non-ulcer dyspepsia
GERD

Front 178

What is the difference between an acute and chronic ulcer?

Back 178

Fibrosis! Absent in acute; dense fibrosis at the base of the ulcer in chronic

Front 179

What is the difference between an erosion and an ulcer? What is the prognosis for each?

Back 179

Erosion: does not breach the muscularis mucosa; may heal
Ulcer: breaches the muscularis mucosa; does not heal

Front 180

H. pylori infection most frequently causes PUD in which area?

Back 180

Duodenum

Front 181

NSAID use most frequently causes PUD in which area?

Back 181

Stomach

Front 182

What are three possible causes of PUD?

Back 182

H. pylori infection; NSAID use; hypersecretory use

Front 183

What are three ways to diagnose PUD?

Back 183

Barium swallow X-ray
Endoscopy with biopsy & cytology
Lab tests

Front 184

When is endoscopy indicated for PUD?

Back 184

When malignancy is suspected - definitively differentiate benign from malignant ulcer

Front 185

What are three indications of a benign ulcer on barium swallow X-ray?

Back 185

Hampton's line; collared border; incisura

Front 186

What are two indications of a malignant ulcer on barium swallow X-ray?

Back 186

Masses; disruption of mucosal folds

Front 187

What is Hampton's line?

Back 187

Radiolucent line across the neck of an ulcer during barium X-ray; indicates mucosal edema

Front 188

Name four tests for H. pylori.

Back 188

Urea breath test; stool Ag; ELISA serology; endoscopic bx

Front 189

Lab tests may be used to rule out which four conditions in peptic ulcer dz?

Back 189

H. pylori; GI bleed; Zollinger Ellison Sd; hyperparathyroidism

Front 190

Name four lab tests and the specific form of peptic ulcer disease each is meant to rule out.

Back 190

Stool Ag (H. pylori)
Hematocrit (GI bleed)
Serum gastrin (Zollinger Ellison Sd)
Serum Ca (hyperparathyroidism)

Front 191

Give the classical clinical description of peptic ulcer disease.

Back 191

Intermittent vague mid epigastric pain related to acid cycles with onset 1-3 hours after eating and frequent night pain

Front 192

Why might food relieve OR exacerbate pain in peptic ulcer disease?

Back 192

Depends on location:
- pain is GREATER (with food) in GASTRIC ulcer
- pain is DECREASED (with food) in DUODENAL ulcer

Front 193

What two things might relieve pain in peptic ulcer disease?

Back 193

Antacids; Vomiting

Front 194

What is MCC dyspepsia?

Back 194

Non-ulcer (functional) dyspepsia

Front 195

Which types of ulcers bleed more commonly: gastric or duodenal?

Back 195

Duodenal

Front 196

Name three major complications of peptic ulcer disease.

Back 196

Bleeding (most common); perforation; obstruction

Front 197

What is the most common complication of PUD?

Back 197

Hemorrhage

Front 198

Describe non-ulcer (functional) dyspepsia.

Back 198

Intermittent epigastric pain related to eating without any organic pathology

Front 199

Describe the clinical manifestation of PUD → perforation.

Back 199

Severe localized epigastric pain → rapid evolution to generalized abdominal pain

Front 200

Peptic ulcer perforation is usually preceded by what?

Back 200

Intensification of ulcer Sx

Front 201

What is frequently required for repair of a perforated peptic ulcer?

Back 201

Surgery

Front 202

Which form of peptic ulcer disease is most likely to cause obstruction? Proximal or distal?

Back 202

Duodenal ulcer → proximal bowel obstruction

Front 203

What are the symptoms of a bowel obstruction caused by peptic ulcer disease?

Back 203

Evolution from ulcer pain → constant pain not relieved by eating
May also present with frequent & high-volume vomiting

Front 204

What is required to establish the diagnosis of PUD obstruction?

Back 204

NG tube

Front 205

Name four possible treatments for PUD obstruction.

Back 205

NG suction; volume/electrolyte replacement; increasing calorie intake; surgery

Front 206

Generally, what are the two steps in treating peptic ulcer disease?

Back 206

Heal the ulcer/relieve the pain
Eliminate the cause

Front 207

What drug(s) should be used for healing peptic ulcer disease?

Back 207

PPI or H2 blocker

Front 208

What is the treatment for H. pylori infection causing PUD?

Back 208

(PPI/bismuth + 2 abx) BID x 14 d

Front 209

What is the treatment for NSAID-induced PUD?

Back 209

Stop the NSAIDs

Front 210

For whatever reason, your NSAID-induced PUD patient must stay on their NSAIDs. What should you give?

Back 210

Misoprostol (PGE1 analogue)

Front 211

What is misoprostol used for in the GI tract?

Back 211

NSAID-induced PUD where the NSAIDs may not be stopped

Front 212

What is the treatment for PUD caused by a hypersecretory state?

Back 212

Resect the gastrin-secreting pancreatic tumor

Front 213

Name one systemic and three non-systemic antacids.

Back 213

Systemic: NaHCO3
Nonsystemic: aluminum salt; magnesium salt; calcium salt

Front 214

Antacids are indicated in what four conditions?

Back 214

Chronic pancreatitis; GERD; peptic ulcer disease; non-ulcer dyspepsia

Front 215

In what condition are antacids but NOT H2R blockers indicated?

Back 215

Chronic pancreatitis

Front 216

What are the side effects of NaHCO3?

Back 216

Alkalinization of blood and urine; kidney stones

Front 217

Aluminum antacids may produce what two side effects?

Back 217

Constipation; hypophosphatemia

Front 218

Magnesum antacids may produce what side effect?

Back 218

Diarrhea

Front 219

Calcium antacids may produce what side effects?

Back 219

Constipation; hypercalcemia

Front 220

When should antacids be given?

Back 220

1 hour after a meal

Front 221

All antacids may cause what side effect?

Back 221

Hypokalemia

Front 222

Histamine H2R blockers are best used to treat what three conditions?

Back 222

Peptic ulcer dz; non-ulcer dyspepsia; GERD

Front 223

In which drugs for PUD are you concerned about crossing the placenta and BBB?

Back 223

Cimetidine

Front 224

Give five toxicities associated with cimetidine.

Back 224

Inhibition of cytochrome P450 (increased levels of other drugs)
Crosses placenta (be careful in pregnancy)
Crosses BBB (→ confusion in sick elderly)
Renal toxicity (↓ creatinine clearance)
Anti-androgen effects (gynecomastia/impotence)

Front 225

Why is sporadic use of cimetidine better than continuous use?

Back 225

Risk of pharmacological tolerance developing

Front 226

Cimetidine may appear in what bodily fluid?

Back 226

Breast milk

Front 227

Why must pregnancy (or risk of) be evaluated in H2R blocker use?

Back 227

Crosses placenta; may appear in breast milk

Front 228

Mucosal protective agents are most useful for what purpose?

Back 228

Increasing ulcer healing (and preventing further damage)

Front 229

Name two mucosal protective agents.

Back 229

Bismuth; sucralfate

Front 230

When should mucosal protective agents be given?

Back 230

Empty stomach

Front 231

Name two side effects of sucralfate.

Back 231

Constipation; bezoar formation

Front 232

What must be prescribed simultaneously with misoprostol? In whom? Why?

Back 232

OCP (in women of reproductive age); misoprostol is a known teratogen and abortifacient

Front 233

Misoprostol is NOT used in what condition?

Back 233

Non-ulcer (functional) dyspepsia

Front 234

Give two other clinical, non-GI uses of misoprostol.

Back 234

Maintain a patent ductus arteriosus in ductus dependent congenital malformations
Induce labor

Front 235

What is one GI side effect of misoprostol?

Back 235

Diarrhea

Front 236

What drug used to treat PUD may also help control ZE Sx?

Back 236

PPI

Front 237

In addition to PUD, NUD, and GERD, what may PPIs treat?

Back 237

ZE Sx
GI bleeding (when given IV)

Front 238

Describe the micro appearance of the normal esophagus.

Back 238

Mucosa: squamous epithelium
Submucosa: upper 2/3 has no glands; lower 1/3 has esophageal mucous glands
Muscularis propria (muscularis externa)
Serosa is NOT present!

Front 239

What is the vascular supply of the esophagus?

Back 239

Mediastinum

Front 240

Is serosa present or absent in the esophagus? How does this affect tumor spread?

Back 240

Absent - one fewer barrier to tumor spread

Front 241

What is the innervation of the esophagus?

Back 241

PSNS/motor: vagus n.
SNS branches

Front 242

Where are submucosal glands present in the esophagus? What do they produce?

Back 242

Present in lower 1/3; produce mucus

Front 243

What kinds of muscle are present in the esophagus?

Back 243

Upper 1/3: skeletal (continuation of cricothyroid muscles)
Middle 1/3: mixed skeletal & smooth
Lower 1/3: smooth muscle only

Front 244

Define esophageal atresia. Where is the most common location?

Back 244

Congenital failure of development of the esophageal cord (blind ended pouch)
Most common location: tracheal bifurcation

Front 245

What is the most common form of esophageal atresia or tracheoesophageal fistula?

Back 245

Upper esophagus atresia + tracheoesophageal fistula at the tracheal bifurcation

Front 246

Define tracheoesophageal fistula.

Back 246

Congenital failure to separate digestive and respiratory tracts

Front 247

Tracheoesophageal fistula is associated with __ in utero.

Back 247

Polyhydramnios

Front 248

What is the typical presentation of tracheoesophageal fistula? In what age group?

Back 248

Salivation, vomiting, coughing, suffocation, cyanosis
Presents in newborn

Front 249

Define achalasia.

Back 249

Persistent contraction of LES
Absence of esophageal peristalsis

Front 250

What is the predominant symptom of achalasia?

Back 250

Progressive dysphagia

Front 251

Give one possible side effect of a PPI.

Back 251

Decreased Ca absorption → osteoperosis

Front 252

Name two drug interactions with a PPI.

Back 252

Clopidogrel (anti-platelet agent)
Increases levels of phenytoin/warfarin (cytochrome inhibitor)

Front 253

When is the IV form of a PPI given?

Back 253

To decrease GI bleeding

Front 254

What is the onset of relief after a PPI is given?

Back 254

24-48 hours

Front 255

Describe the mechanism of a PPI.

Back 255

Irreversibly binds and deactivates H/K ATPase on lumenal side of parietal cell

Front 256

What are the valves of Kerkring?

Back 256

Plica circulares; gross small intestinal mucosal appearance

Front 257

What three cells are found in the villi of the small intestinal mucosa?

Back 257

Enterocytes; goblet cells; endocrine cells

Front 258

What four cells are found in the crypts of the small intestinal mucosa?

Back 258

Precursor (stem/neck) cells; columnar cells; Paneth cells; endocrine cells

Front 259

Paneth cells are primarily responsible for secreting __.

Back 259

lysozyme

Front 260

Name five developmental diseases of the small intestine.

Back 260

Malrotation; stenosis; duodenal atresia; diverticula; Meckel's diverticulum

Front 261

Name two conditions associated with duodenal atresia. Name another congenital GI condition associated with each.

Back 261

Down's Syndrome; Hirschprung's disease
Polyhydramnios; pyloric stenosis

Front 262

What are the SSx of duodenal atresia?

Back 262

Early (at birth) bilious vomiting; proximal stomach distention

Front 263

What sign on X-ray is typical of duodenal atresia?

Back 263

Double bubble (one bubble in stomach, one bubble in duodenum)

Front 264

How do diverticula and polyps differ?

Back 264

Diverticulum: sac pushes outward from lumen
Polyp: solid mass pushes into the lumen

Front 265

Diverticula of the small intestine are often __ in the duod and __ in the jejunum.

Back 265

single; multiple

Front 266

Meckel's diverticulum is a remnant of __.

Back 266

omphalomesenteric duct

Front 267

What is the rule of 2s? To what condition does it apply?

Back 267

Meckel's diverticulum:
- 2 feet (or ess) proximal to ileocecal valve
- 2 inches in length
- 2% of the population
- 2 types of ectopic epithelium (pancreatic, esophageal)
- 2 yo at presentation

Front 268

What is the most common congenital anomaly of the GI tract?

Back 268

Meckel's diverticulum

Front 269

The omphalomesenteric duct is also known by what two names?

Back 269

Vitelline duct; yolk sac

Front 270

What is the MCC small bowel obstruction?

Back 270

Recent surgery → adhesion

Front 271

Give the presentation of an adhesion in the small bowel.

Back 271

Acute bowel obstruction, most commonly from a recent surgery

Front 272

Describe the micro appearance of an adhesive small bowel obstruction.

Back 272

Well-demarcated necrotic zones

Front 273

Give four examples of obstructive diseases of the small intestine.

Back 273

Adhesion; hernia; intussusception; volvulus

Front 274

Describe the gross appearance of intussusception.

Back 274

Telescoping of one segment of bowel into another (usually ileum into cecum)

Front 275

What is the most common location of intussusception?

Back 275

Ileum into cecum

Front 276

In what group is intussusception most common?

Back 276

Infants

Front 277

Intussusception is frequently caused by __ in adults.

Back 277

intralumenal polyp or mass

Front 278

Intussusception is frequently caused by intralumenal polyps or masses in what group?

Back 278

Adults

Front 279

Give three complications of intussusception.

Back 279

Ischemia, infarction, perforation

Front 280

Volvulus is most common in what group?

Back 280

Elderly

Front 281

What is volvulus?

Back 281

Twisting of bowel loop around its mesentery

Front 282

In what area of the GI tract is volvulus most common? Why?

Back 282

Sigmoid colon; redundant mesentery

Front 283

Give three complications of volvulus.

Back 283

Ischemia, infarction, perforation

Front 284

What are three important signs of malabsorptive diseases?

Back 284

Unexplained weight loss; anorexia; steatorrhea/oily diarrhea

Front 285

What are the three mechanisms of malabsorptive diseases?

Back 285

Poor digestion: inability to break down food
Poor absorption: blunting of villi
Poor transport: lymphatic obstruction

Front 286

Name three causes of malabsorptive disease in which poor digestion is the culprit.

Back 286

Pancreatic insufficiency; bile salt deficiency; bacterial overgrowth

Front 287

Name three causes of malabsorptive disease in which poor absorption is the culprit.

Back 287

Infection; celiac disease; small bowel disease

Front 288

Name three causes of malabsorptive disease in which poor transport is the culprit.

Back 288

Lymphoma; TB; lymphangiectasia

Front 289

Describe the micro appearance of celiac disease.

Back 289

Blunting of villi; crypt elongation; lymphocytic infiltrate in epithelial cells and lamina propria

Front 290

Describe the gross appearance of celiac disease. Where is it most severe?

Back 290

Cerebriform velvety mucosa; most severe in duod & jejunum

Front 291

Describe the etiology of celiac disease.

Back 291

CD4 mediated (type IV) hypersensitivity rxn to gliadin (found in gluten) → mucosal damage

Front 292

Describe the epidemiology of celiac disease.

Back 292

Onset in childhood; more common in females

Front 293

What HLA haplotypes are most associated with celiac disease?

Back 293

DQ2 or DQ8

Front 294

What dermatological abnormality is associated with celiac disease?

Back 294

Dermatitis herpetiformis

Front 295

Celiac disease causes high risks of what two conditions?

Back 295

T cell lymphoma; small bowel adenocarcinoma

Front 296

What two lab tests can diagnose celiac disease? What clinical test can diagnose celiac disease?

Back 296

Anti-tissue transglutaminase; anti-endomysial IgA Ab
Gluten free diet → improved clinical & pathological Sx

Front 297

Name six clinical manifestations of celiac disease.

Back 297

Diarrhea; malabsorption; weight loss; iron deficiency anemia; osteoperosis; peripheral neuromuscular disorders

Front 298

How do you treat tropical sprue?

Back 298

Broad spectrum abx; B12 + folate supplementation

Front 299

What is the major clinical feature of tropical sprue?

Back 299

B12 deficiency → pernicious anemia

Front 300

The gross pathology of tropical sprue is most severe in which region of the GI tract?

Back 300

Ileum (distal small bowel)

Front 301

Malabsorptive disease concentrated in the __ is most likely to be celiac disease, while disease concentrated in the __ is likely to be tropical sprue.

Back 301

duodenum & jejunum; ileum

Front 302

Malabsorptive disease concentrated in the proximal small bowel is most likely to be __, while disease concentrated in the distal small bowel is likely to be __.

Back 302

celiac disease; tropical sprue

Front 303

What is Whipple's disease? What is its etiology?

Back 303

Multi-system dz with malabsorption & anemia; caused by Gram +ve actinomycete Tropheryma whipelli

Front 304

How do you treat Whipple's disease?

Back 304

Broad spectrum abx

Front 305

What do you see on EM in Whipple's disease?

Back 305

Small, rod-like bacteria

Front 306

What do you see on stain in Whipple's disease?

Back 306

PAS+ve, AFB -ve foamy mΦ with bacterial particles

Front 307

If a stain of GI pathology is AFB positive, what disease should you consider?

Back 307

Disseminated MAC

Front 308

Describe the gross appearance of adenocarcinoma of the small intestine.

Back 308

Napkin ring pattern encircling; may lead to obstruction

Front 309

What is important prognostically about adenocarcinoma of the small intestine?

Back 309

Often metastasized already by time of dx

Front 310

Put these adenocarcinomas in order of prevalence: gastric, small intestine, colon

Back 310

Large intestine >>> gastric >> small intestine

Front 311

Why should adenocarcinoma of the small intestine be relatively low on your DDx?

Back 311

Rare!

Front 312

Compare the prognosis of ampulla of Vater adenoCa with pancreatic adenoCa.

Back 312

Ampulla of Vater adenoCa prognosis is much better

Front 313

In ampulla of Vater adenoCa, what correlates most closely with prognosis?

Back 313

TNM staging

Front 314

What is the typical presentation of ampulla of Vater adenoCa? This is similar to what other condition?

Back 314

Early painless jaundice; similar to pancreatic head tumors

Front 315

Carcinoid tumors of the small intestine are similar to what other tumor? How so?

Back 315

Small cell lung Ca; tumor of neuroendocrine cells

Front 316

What is the most common location of carcinoid tumors of the GI tract?

Back 316

Small intestine

Front 317

What is the prognosis of carcinoid tumors?

Back 317

Relatively good; all are malignant, but of low-grade potential

Front 318

Name three clinical manifestations of carcinoid tumors of the GI tract.

Back 318

Flushing; Diarrhea; Right-sided valvular lesions

Front 319

Flushing in carcinoid tumor symptoms is due to what?

Back 319

Serotonin (5HT)

Front 320

Describe the micro appearance of carcinoid tumors.

Back 320

Well organized, uniform cells with salt and pepper chromatin

Front 321

Name two IHC markers typically seen in carcinoid tumors.

Back 321

Chromogranin, synaptophysin (both neuroendocrine markers)

Front 322

Compare the prognosis of carcinoid tumors across the GI tract and with that of adenoCa.

Back 322

Better prognosis than adenocarcinoma
Worse prognosis (more aggressive) in jejunum & ileum
Relatively benign everywhere else in the GI tract

Front 323

In the stomach, carcinoid tumors are associated with __.

Back 323

atrophic gastritis

Front 324

In the duodenum, carcinoid tumors are associated with __.

Back 324

Zollinger-Ellison Syndrome

Front 325

Name three substances secreted by a carcinoid tumor in the small intestine.

Back 325

Serotonin; Polypeptide YY; Substance P

Front 326

Name three substances secreted by a carcinoid tumor in the duodenum.

Back 326

Somatostatin; Gastrin; CCK

Front 327

What is the typical size of a carcinoid tumor lesion in the jejunum/ileum?

Back 327

Large (>2 cm)

Front 328

Name three substances secreted by a carcinoid tumor in the stomach.

Back 328

Somatostatin; Histamine; Serotonin

Front 329

What are the four steps in fat absorption? What enzymes catalyze the first two steps?

Back 329

Pancreatic (lipolytic): pancreatic lipase
Hepatobiliary (solubilization): bile
Mucosal (absorptive)
Intracellular (lymphatic)

Front 330

What happens in each step of fat absorption?

Back 330

Pancreatic: TG → FA + MG
Hepatobiliary: micelle forms → FA + MG emulsified
Mucosal: micelle disintegrates → enters cell; FA + MG → TG
Intracellular: TGs clump together → chylomicron → transported away via lymphatics

Front 331

The vast majority of protein is digested by __ enzymes.

Back 331

pancreatic

Front 332

What is the definition of malabsorption?

Back 332

Failure of normal fat absorption → steatorrhea

Front 333

Name four clinical manifestations of malabsorption.

Back 333

Weight loss
Steatorrhea
Nitrogen malabsorption (creatorrhea)
Vitamin deficiencies

Front 334

What is the first test to confirm the dx of malabsorption?

Back 334

Quantitative fecal fat

Front 335

How is a quantitative fecal fat test performed?

Back 335

Give fixed diet including 100g fat over 3 days. If fat excretion > 6g → dx malabsorption

Front 336

There is a __ relationship between fat intake and fat excretion.

Back 336

linear

Front 337

What surgical procedure will lead to increased fat excretion?

Back 337

Ileal resection > 100 cm

Front 338

What does a D-xylose test measure?

Back 338

Proximal intestinal function (no digestion required)

Front 339

How is a D-xylose test performed?

Back 339

Give PO D-xylose → collect urine. Normal: > 5g excretion via urine

Front 340

What is one complication of the D-xylose test?

Back 340

Results in pt in renal failure will be sub-optimal

Front 341

What is another name for Schilling's test?

Back 341

B12 absorptive test

Front 342

What does Schilling's test measure?

Back 342

Distal intestinal function

Front 343

How is Schilling's test performed?

Back 343

Step 1: give non-irradiated ("cold") B12 to saturate tissue binding sites
Step 2: give irradiated ("hot") B12 + (in sequence):
- nothing (give hot B12 alone)
- oral intrinsic factor
- abx
- pancreatic enzymes

Front 344

If Schilling's test normalizes after giving hot oral B12 alone, what does this indicate?

Back 344

Food cobalamin malabsorption

Front 345

If Schilling's test normalizes after giving hot oral B12 + PO intrinsic factor, what does this indicate?

Back 345

Pernicious anemia

Front 346

If Schilling's test normalizes after giving hot oral B12 + abx, what does this indicate?

Back 346

Bacterial overgrowth

Front 347

If Schilling's test normalizes after giving hot oral B12 + pancreatic enzymes, what does this indicate?

Back 347

Pancreatic insufficiency

Front 348

What is considered "normal" in a Schilling test?

Back 348

> 7% of oral B12 should be found in the urine within 24 hours

Front 349

What does the bile salt C14 breath test diagnose?

Back 349

Small bowel stasis 2/2 bacterial overgrowth

Front 350

How is the Bile salt C14 breath test performed?

Back 350

Give PO bile acid (conjugated to C14 taurine)
Measure CO2-14 after bacteria deconjugates bile acid in small bowel
Bacterial overgrowth → too much deconjugation → increased CO2-14 in breath

Front 351

What is the diagnostic test of choice in celiac disease?

Back 351

Small bowel biopsy

Front 352

What is the diagnostic test of choice in Whipple's disease?

Back 352

Small bowel biopsy

Front 353

What is the diagnostic test of choice in a-beta-lipoproteinemia?

Back 353

Small bowel biopsy

Front 354

Small bowel biopsy is the diagnostic test of choice for what three conditions?

Back 354

Celiac disease; Whipple's disease; A-beta-lipoproteinemia

Front 355

Small bowel X-ray is most effective in looking for what condition?

Back 355

Obstruction

Front 356

What is the most common disaccharidase deficiency?

Back 356

Lactase deficiency (aka lactose intolerance)

Front 357

How do you diagnose lactose intolerance?

Back 357

Lactose tolerance test

Front 358

What are mild, moderate, and severe responses to the lactose tolerance test?

Back 358

Mild: abdominal distention
Moderate: severe distention with loose stools
Severe: osmotic diarrhea

Front 359

Name five etiologies of pancreatic exocrine insufficiency.

Back 359

Chronic pancreatitis; ductal blockage 2/2 pancreatic carcinoma; CF; pancreatic resection; Zollinger-Ellison Sd

Front 360

How does Zollinger Ellison Syndrome create pancreatic insufficiency?

Back 360

Increased gastrin production → lower gastric pH → lower duodenal pH → pH inactivation of pancreatic lipase

Front 361

How do you treat exocrine pancreatic insufficiency?

Back 361

Replace pancreatic enzymes; if ZE, fix pH problems

Front 362

Name four etiologies of bile salt insufficiency.

Back 362

Biliary obstruction; blind loop syndrome; ileal resection; ZE

Front 363

How do you treat bile salt insufficiency?

Back 363

Depends on cause
- obstruction: remove
- ZE: fix pH problems
- all: replace bile salts

Front 364

What is blind loop syndrome?

Back 364

Obstruction → bacterial overgrowth of small intestine → ineffective bile salt activity

Front 365

What are the two peaks of celiac disease?

Back 365

Infancy and middle age

Front 366

Refractory iron deficiency anemia may be due to what cause?

Back 366

Celiac disease

Front 367

How does Crohn's disease cause malabsorption?

Back 367

Often causes problems in the terminal ileum → presents with watery diarrhea ± RLQ colicky pain (2/2 small bowel obstruction in terminal ileum)

Front 368

Hirschprung's disease has a higher frequency in __ patients.

Back 368

Down's syndrome

Front 369

What two GI manifestations are common in Down's syndrome patients?

Back 369

Hirschprung's disease; duodenal atresia

Front 370

What is the cause of congenital megacolon?

Back 370

Absence of ganglion cells in Meissner's and Auerbach's plexi in distal colon

Front 371

In which part of the colon does Hirschprung's typically develop?

Back 371

Distal colon

Front 372

Name four clinical manifestations of Hirschprung's disease.

Back 372

Constipation; abdominal distention; vomiting; failure to pass meconium (neonate)

Front 373

How do you diagnose Hirschprung's disease?

Back 373

Rectal biopsy (confirm absence of ganglia)

Front 374

What is the difference between diverticulosis and diverticulitis?

Back 374

Diverticulosis: formation of diverticula
Diverticulitis: inflammation 2/2 obstruction of diverticulum, usually by fecalith

Front 375

Where does diverticulosis most typically occur?

Back 375

Sigmoid colon

Front 376

What is MCC hematochezia?

Back 376

Diverticulosis

Front 377

In what age group is diverticulosis most common?

Back 377

Elderly (60+)

Front 378

How does diverticulitis typically present?

Back 378

LLQ appendicitis

Front 379

Give four possible complications of diverticulosis.

Back 379

Hematochezia; diverticulitis; abscess → fistula formation; colonic obstruction

Front 380

Describe melanosis coli.

Back 380

Asymptomatic brown discoloration of colonic mucosa

Front 381

Melanosis coli is associated with what two substances?

Back 381

Senna; cascara sagrada

Front 382

What is the most likely infectious cause of peritonitis in an adult?

Back 382

E. coli

Front 383

What is the most likely infectious cause of peritonitis in a child with nephrotic symptoms?

Back 383

Pneumococcus

Front 384

Give three possible chemical causes of peritonitis.

Back 384

Gastric perforation; gallbladder perforation; hemorrhagic pancreas with pseudocyst

Front 385

Give three possible inflammatory causes of peritonitis.

Back 385

Appendicitis; diverticulitis; cholecystitis

Front 386

Give three possible etiologies of hemorrhoids.

Back 386

Constipation; pregnancy (venous stasis); portal HTN

Front 387

What is the difference between an internal and external hemorrhoid in terms of location and Sx?

Back 387

Internal: above anorectal line; not painful, blood in the stool
External: below anorectal line; painful, thrombosis

Front 388

What are the two forms of ischemic bowel disease? What causes each?

Back 388

Transmural: caused by acute ischemia
Mucosal: caused by hypoperfusion 2/2 CHF, dehydration

Front 389

What causes the greatest amount of injury in ischemic bowel dz?

Back 389

Reperfusion injury after relief of ischemia

Front 390

Give two possible consequences of reperfusion injury in ischemic bowel dz.

Back 390

Hemorrhage; obstruction

Front 391

What two areas are the most vulnerable to ischemic bowel dz? Why?

Back 391

Watershed areas: splenic flexure and rectosigmoid jxn

Front 392

What are the classical SSx of a splenic flexure infarct?

Back 392

Localized LUQ pain with bloody diarrhea

Front 393

What are the classical SSx of a small bowel infarct?

Back 393

Generalized periumbilical pain with bloody diarrhea

Front 394

Ischemic bowel disease most typically occurs in what age group?

Back 394

Elderly

Front 395

Necrotizing enterocolitis typically occurs in what age group?

Back 395

Preemies

Front 396

What is necrotizing enterocolitis?

Back 396

Necrosis of intestinal mucosa

Front 397

What is the 2nd MCC of hematochezia?

Back 397

Angiodysplasia

Front 398

Describe angiodysplasia.

Back 398

Tortuous dilation of small vessels of intestinal mucosa or submucosa

Front 399

Where does angiodysplasia most typically occur?

Back 399

Cecum & ascending colon (right side)

Front 400

What infectious diseases may mimic inflammatory bowel diseases?

Back 400

TB proctocolitis (mimics Crohn's); Campylobacter jejuni colitis (mimics UC)

Front 401

Long-term complications of either inflammatory bowel disease may include what?

Back 401

Colitis associated neoplasia

Front 402

What is the standard treatment for low-grade dysplasia in inflammatory bowel patients?

Back 402

Colectomy

Front 403

What is the standard treatment for high-grade dysplasia in inflammatory bowel patients?

Back 403

Colectomy

Front 404

When does the risk of dysplasia occur in inflammatory bowel disease patients?

Back 404

8 years after disease initiation and pancolitis

Front 405

Endoscopy and biopsy are standard how long after diagnosis of an inflammatory bowel disease? Why?

Back 405

8 years - after 8 years, risk of dysplasia increases

Front 406

What is the most common type of polyp?

Back 406

Hyperplastic polyps

Front 407

What is the clinical significance of hyperplastic polyps?

Back 407

NONE! Benign and asymptomatic

Front 408

When are hyperplastic polyps usually found? Where in the GI tract?

Back 408

Incidental finding on endoscopy; left colon (rectosigmoid)

Front 409

Inflammatory pseudopolyps are typically found in what condition?

Back 409

Chronic ulcerative colitis

Front 410

What are inflammatory pseudopolyps made of?

Back 410

Gradulation tissue and regenerating mucosa

Front 411

Where do benign lymphoid polyps typically occur?

Back 411

Rectum

Front 412

What are the two types of juvenile polyps in the colon? What is the prognosis of each?

Back 412

Sporadic: solitary polyps, typically benign
Inherited: 3-100 polyps, pre-cancerous

Front 413

Where are juvenile polyps typically found?

Back 413

Rectum

Front 414

When are juvenile polyps typically found?

Back 414

Cause rectal bleeding (found on investigation of rectal bleed)

Front 415

Describe the pathologic appearance of juvenile polyps.

Back 415

Hamartomatous; dilated crypts filled with mucin

Front 416

What type of polyps are Peutz-Jeghers polyps?

Back 416

Hamartomas

Front 417

Describe the manifestations of Peutz-Jeghers syndrome.

Back 417

Polyps in colon & small intestine; malanotic accumulations in mouth, lips, hands, and genitalia

Front 418

The dermatologic manifestations of Peutz-Jeghers syndrome are known as __.

Back 418

childhood lentigines

Front 419

Describe the gross appearance of the polyps associated with Peutz-Jeghers Sd.

Back 419

Large pedunculated hamartomatous polyps

Front 420

Describe the micro appearance of the polyps associated with Peutz-Jeghers Sd.

Back 420

Branching, tree-like network of smooth muscle cells and connective tissue

Front 421

When does surveillance for colorectal cancer begin?

Back 421

Age 45 in African-Americans; age 50 in all others

Front 422

What is the most common type of adenomatous polyp?

Back 422

Tubular adenoma

Front 423

What is the prognosis of a tubular adenoma?

Back 423

Benign in itself, but may undergo malignant change

Front 424

Describe the gross appearance of a tubular adenoma.

Back 424

Small pedunculated polyp. Surface kind of looks like brain coral.

Front 425

Compare tubular and villous adenomas.

Back 425

Tubular: more common, lower potential for malignant change
Villous: less common, high potential for malignant change

Front 426

Describe the gross appearance of a villous adenoma.

Back 426

Large sessile tumor with velvety surface with villi-like projections

Front 427

Describe the gross appearance of a serrated adenoma.

Back 427

Sessile tumor with serration

Front 428

Describe the micro appearance of a serrated adneoma.

Back 428

Resembles hyperplastic polyp + dysplasia

Front 429

What is the difference between a hyperplastic polyp and a serrated adenoma?

Back 429

Serrated adenoma has dysplasia → risk of malignancy

Front 430

Why are sessile serrated polyps frequently called adenomas? Why don't they really qualify?

Back 430

Pre-malignant lesions associated with adenoCa development
Do NOT have any dysplasia (so not "true" adenomas)

Front 431

Describe the characteristic appearance of a sessile serrated polyp.

Back 431

Dilated crypt base with lateral growth; flat lesions grossly

Front 432

How does an intramucosal adenoCa differ from intraepithelial adenoma, micro and prognostically?

Back 432

Dysplastic epithelial cells invade lamina propria, muscularis mucosa, or submucosa
Increased risk of metastasis

Front 433

What gene is associated with familial adenomatous polyposis?

Back 433

APC (tumor suppressor gene)

Front 434

Describe the natural history of a patient with FAP.

Back 434

Present at birth with colon polyposis; usually dx with colon cancer by age 30

Front 435

What is the treatment for FAP?

Back 435

Prophylactic total colectomy

Front 436

What is the risk of malignant transformation in FAP?

Back 436

100%. It will happen unless the person dies of something else first.

Front 437

What is Gardner syndrome? What is its inheritance pattern?

Back 437

FAP + benign osseous and soft tissue tumors (osteomas, epidermal cysts, fibromatosis)
Autosomal dominant with variable penetrance

Front 438

What is Turcot syndrome?

Back 438

FAP + CNS tumor (glioblastoma)

Front 439

What is another name for Lynch syndrome?

Back 439

Hereditary non-polyposis colorectal cancer

Front 440

How does Lynch syndrome typically present?

Back 440

Right sided colon cancer at a young age

Front 441

Describe the gross appearance of FAP in the colon.

Back 441

100+ polyps "carpet" the entire colon, usually spanning the entire length (± rectum, based on family hx)

Front 442

What is the genetic basis for Lynch syndrome?

Back 442

Mutation in mismatch repair → microsatellite instability
Autosomal dominant

Front 443

What are the Amsterdam criteria? What dz are they used to identify?

Back 443

Used to identify high-risk patients for HNPCC (Lynch Sd)
- 3+ family members with confirmed dx of CRC, 1+ of whom is a 1° relative of the other two
- 2+ affected generations
- 1+ affected at under age 50
- exclusion of FAP

Front 444

What are the two patterns of CRC? Where does each pattern typically develop?

Back 444

Napkin ring (annular) pattern: left colon
Polypoid (fungating) pattern: right colon

Front 445

What is the typical side effect of a "napkin ring" pattern in CRC?

Back 445

Obstruction

Front 446

What is the typical side effect of a "polypoid" pattern in CRC?

Back 446

Bleeding (often occult)

Front 447

Name five factors which might predispose a person to CRC.

Back 447

Adenomatous polyps; inherited multiple polyposis syndrome; chronic ulcerative colitis; family hx (genetics); low-fiber high fat diet

Front 448

What is carcinoembryonic antigen used for? What can it NOT be used for?

Back 448

Can be used to monitor progression
Can NOT be used for Dx!

Front 449

Describe the typical pathogenesis of sporadic colon cancer.

Back 449

APC/beta-catenin pathway → chromosomal instability

Front 450

Which form(s) of colorectal cancer are associated with DNA mismatch repair?

Back 450

Lynch Syndrome

Front 451

Which form(s) of colorectal cancer are associated with APC or the beta-catenin pathway?

Back 451

Sporadic CRC or FAP

Front 452

What are three variants of the micro appearance of CRC? How do these differ in prognosis?

Back 452

Intestinal adenocarcinoma (better prognosis)
Mucinous type (worse prognosis)
Signet ring cell (diffuse) type (worse prognosis)

Front 453

Give two typical clinical manifestations of left-sided colon cancer.

Back 453

Diarrhea; constipation

Front 454

Give two typical clinical manifestations of right-sided colon cancer.

Back 454

Iron deficiency anemia; weight loss

Front 455

Prognosis in CRC is best associated with what?

Back 455

TNM staging

Front 456

Stage 4 colon cancer is defined by what?

Back 456

Metastasis to the liver

Front 457

Stage 3 colon cancer is defined by what?

Back 457

Metastasis to 1+ regional lymph node (but NOT the liver!)

Front 458

Stage 2+ tumors should be treated how?

Back 458

Chemo

Front 459

What is the most common site of distant metastasis of colon cancer? What two cancers in CRC do not show this pattern?

Back 459

Liver (via portal circulation)
Anal & rectal cancers do not typically met to liver

Front 460

What is the most common tumor of the appendix? Where is it typically found?

Back 460

Low-grade carcinoid
Found in the distal tip of appendix

Front 461

What is a mucocele?

Back 461

Appendix dilated by intralumenal mucinous secretion

Front 462

What are two kinds of mucoceles? How do they differ?

Back 462

Mucinous cystadenoma: benign
Mucinous adenoCa: malignant

Front 463

What is the pathologic definition of acute appendicitis?

Back 463

Neutrophils in the muscularis propria

Front 464

What is the most important etiologic factor in inflammatory bowel dz?

Back 464

Genetic susceptibility

Front 465

How does IBD develop?

Back 465

Susceptibility → environmental trigger → lumenal microbial Ag → immune response

Front 466

What is the proposed etiology for Crohn's disease?

Back 466

Post-infectious (IgG against Saccharomyces cerevisiae)

Front 467

What is the proposed etiology for chronic UC?

Back 467

Autoimmune (anti-pANCA Ab)

Front 468

How does smoking affect IBD?

Back 468

Crohn's: predisposes or makes it worse
UC: protective; quitting smoking may predispose

Front 469

What is typically seen on barium X-ray in IBD?

Back 469

Crohn's: "string sign"
UC: lead pipe

Front 470

Describe the string sign. In which test is it seen? If your patient has IBD, which type should you suspect?

Back 470

In barium X-ray: extremely narrow intestinal lumen (looks like a "string", rather than a normal lumen)
More typical of Crohn's disease

Front 471

Describe the lead pipe sign. In which test is it seen? If your patient has IBD, which type should you suspect?

Back 471

In barium X-ray: loss of haustral folds ("lead pipe", not normal colon)
More typical of UC

Front 472

Where are the lesions of Crohn's disease located? What areas are spared?

Back 472

May be located anywhere along GI tract (mouth to anus) - "skip" lesions (non-continuous)
Ileum and anus usually affected
Rectum usually spared

Front 473

Where are the lesions of ulcerative colitis located? What areas are spared?

Back 473

Colon ONLY; continuous ascending lesions (rectum → distal → proximal
Rectum usually affected
Anus usually spared

Front 474

Describe the gross appearance of the lesions of Crohn's disease.

Back 474

Transmural inflammation; cobblestone mucosa; creeping fat; bowel wall thickening (and narrowing lumen)

Front 475

Describe the gross appearance of the lesions of ulcerative colitis.

Back 475

Mucosal & submucosal inflammation; friable mucosal pseudopolyps; lots of bleeding, even just on sigmoidoscopy

Front 476

Describe the micro appearance of the lesions of ulcerative colitis.

Back 476

Crypt abscesses; microscopic ulcerations. NO granulomas!

Front 477

Describe the micro appearance of the lesions of Crohn's disease.

Back 477

Non-caseating granulomas; lymphoid aggregates

Front 478

Give three SSx associated with Crohn's disease which may help differentiate it from UC.

Back 478

Colickly RLQ pain
RLQ mass
Watery diarrhea

Front 479

Give three SSx associated with UC which may help differentiate it from Crohn's disease.

Back 479

Crampy abdominal pain
Bloody diarrhea
Rectal bleeding

Front 480

What should be on the DDx for a RLQ pain/mass?

Back 480

Acute appendicitis; Yersinia; ovarian cyst; lymphoma; TB (mostly in developing countries); Crohn's dz

Front 481

What should be on the DDX for exudative diarrhea?

Back 481

Infectious colitis; ulcerative colitis; pseudomembranous colitis; ischemic colitis; left sided CRC

Front 482

Name six possible GI complications of Crohn's disease.

Back 482

Small bowel obstruction (ileal involvement); strictures; fistulas; perforation; abscess; perianal dz

Front 483

Name four possible GI complications of ulcerative colitis.

Back 483

Toxic megacolon; CRC; perforation → hemorrhage; rectal dz

Front 484

Which IBD is a serious risk factor for colorectal cancer?

Back 484

Ulcerative colitis

Front 485

Name four systemic complications of Crohn's dz.

Back 485

Weight loss; erythema nodosum; B12 deficiency → megaloblastic anemia; arthritis

Front 486

Name four systemic complications of ulcerative colitis.

Back 486

Primary sclerosing cholangitis; pyoderma gangrenosum; iron deficiency → anemia; arthritis

Front 487

How do you dx ulcerative colitis?

Back 487

Clincial hx of diarrhea and rectal bleeding
Supportive: biopsy, barium enema

Front 488

How do you dx Crohn's disease?

Back 488

Endoscopy; CT; barium enema

Front 489

How do you tx Crohn's disease?

Back 489

Steroids

Front 490

How do you tx ulcerative colitis?

Back 490

Sulfasalazine; colectomy

Front 491

Why is colectomy curative in ulcerative colitis but not Crohn's dz?

Back 491

Ulcerative colitis is, by definition, confined to the colon. Colectomy will miss some lesions (and in fact, the most common lesion location) in Crohn's dz.

Front 492

What is the definition of diarrhea?

Back 492

>200g stool per day (either >200 gm stool weight or >200 ml fecal H2O per 24 hr)

Front 493

In what type(s) of diarrhea is the stool WBC/RBC positive?

Back 493

Exudative

Front 494

What is the osmotic gap in osmotic diarrhea?

Back 494

>100 mOsm/L

Front 495

In which type(s) of diarrhea does an osmotic gap exist?

Back 495

Osmotic diarrhea

Front 496

What are the two etiologies of osmotic diarrhea? Give an example of each.

Back 496

Osmotic ingestion (sortibol)
Malabsorption (Crohn's disease, lactase deficiency)

Front 497

Describe the pathogenesis of osmotic diarrhea.

Back 497

Increased amount of osmotically active, poorly absorbed substances in the gut → pulls all the water out → diarrhea

Front 498

How do you calculate the osmotic gap?

Back 498

2 ([Na] + [K])
If acutal - calculated > 50 → abnormal!!

Front 499

How much water can the small intestine absorb daily? Large intestine?

Back 499

12 L in small intestine; 6 L in large intestine

Front 500

What is the diarrhea work-up?

Back 500

Fecal smear of stool (looking for leukocytes)
- Positive (exudative diarrhea): Cx
* If Cx positive: Gram stain (find the bug)
* If Cx negative: colonoscopy + bx (cancer, colitis, IBD)
- Negative: osmotic gap in stool
* If osmotic gap > 100 mOsm/L, osmotic diarrhea
* If osmotic gap normal, secretory diarrhea

Front 501

What should NEVER be used in the dx of diarrhea?

Back 501

Barium enema

Front 502

Dermatitis herpetiformis is a systemic manifestation of __.

Back 502

celiac disease

Front 503

Cheilosis, stomatitis, and glossitis (when seen with diarrhea) are systemic manifestations of __.

Back 503

malabsorption

Front 504

Purpura is a systemic manifestation of what GI disorder?

Back 504

Vitamin K deficiency

Front 505

Hyperkeratosis is a systemic manifestation of what GI disorder?

Back 505

Vitamin A deficiency

Front 506

Hyperpgimentation may be a systemic manifestation of what three disorders that may also cause diarrhea?

Back 506

Whipple's dz, celiac dz, Addison's dz

Front 507

Flushing + diarrhea are signs of what two conditions?

Back 507

Carcinoid or VIPoma

Front 508

Name four possible causes of osmotic diarrhea due to osmotic ingestion.

Back 508

Sorbitol, lactulose, mannitol, Mg antacid

Front 509

Name seven possible malabsorptive causes of osmotic diarrhea.

Back 509

Lactase deficiency; pancreatic insufficiency; celiac dz; tropical sprue; Whipple's dz; bug overgrowth; Crohn's dz

Front 510

Give six possible differentialdiagnoses for exudative diarrhea.

Back 510

Infectious colitis; pseudomembranous colitis; ischemic colitis; radiation colitis; inflammatory bowel dz; left sided CRC

Front 511

A patient presents with a large volume of watery diarrhea + fever + RLQ abdominal mass. Dx.

Back 511

Crohn's dz → exudative AND osmotic diarrhea (malabsorption and ulceration)

Front 512

A patient c/o explosive diarrhea and weight loss after habitually chewing gum. Dx.

Back 512

Osmotic diarrhea 2/2 sorbitol ingestion

Front 513

Secretory diarrhea usually occurs when and under what conditions?

Back 513

At night; not triggered by drinking or eating (due to hypersecretion)

Front 514

Give five possible differential diagnoses for secretory diarrhea.

Back 514

Infectious (enterotoxin-mediated); ZE; carcinoid; collagenous colitis; lymphocytic colitis

Front 515

A woman presents with hot flushes and chronic watery diarrhea. Dx. What kind of diarrhea are they experiencing?

Back 515

Carcinoid → secretory diarrhea

Front 516

A young man with family hx of peptic ulcers c/o diarrhea, worse at night and unrelated to eating. Dx. What kind of diarrhea are they experiencing?

Back 516

Zollinger-Ellison Syndrome → secretory diarrhea

Front 517

Describe the likely findings of colon bx in a patient with exudative diarrhea.

Back 517

Ulcerated or inflamed mucosa; leaking blood and pus into lumen

Front 518

An elderly pt with CHF presents with localized LLQ pain and bloody diarrhea. Dx. What kind of diarrhea are they experiencing?

Back 518

Ischemic colitis → exudative diarrhea

Front 519

A patient s/p radiation tx for cancer now c/o bloody diarrhea. Dx. What type of diarrhea are they experiencing?

Back 519

Radiation colitis → exudative diarrhea

Front 520

Describe the pathogenesis of dysmotility diarrhea.

Back 520

Hypomotility → intestinal stasis → bacterial overgrowth; combination of osmotic and secretory diarrhea

Front 521

Give four likely causes of dysmotility diarrhea.

Back 521

Irritable bowel Sd; SLE; rheumatoid arthritis; DM

Front 522

A young woman c/o watery diarrhea and abdominal discomfort. She has experienced no recent unexpected weight loss. Dx.

Back 522

Irritable bowel Sd

Front 523

Which type(s) of diarrhea may be caused by Zollinger Ellison?

Back 523

ALL: gastrin → secretory diarrhea; small bowel irritation (by acid) → exudative diarrhea; malabsorption → osmotic diarrhea

Front 524

Where do "upper" GI bleeds occur? What are the typical Sx of an upper GI bleed?

Back 524

Proximal to ligament of Treitz (4th stage of duod)
Hematemesis; melena

Front 525

Where do "lower" GI bleeds occur? What are the typical Sx of an lower GI bleed?

Back 525

Distal to ligament of Treitz
Hematochezia

Front 526

How do we define "major", "minor", and "occult" GI bleeds?

Back 526

Major: accompanied by hemodynamic instability
Minor: no hemodynamic instability
Occult: not visible grossly (detected on guaiac testing)

Front 527

What is the cardinal rule of GI bleeding?

Back 527

It's life threatening until proven otherwise

Front 528

What are the two "kinds" of hematemesis?

Back 528

Red, fresh blood in vomitus or coffee ground vomitus

Front 529

Coffee ground vomitus is suggestive of what process?

Back 529

Previous upper GI bleed with decently long exposure to gastric acid

Front 530

Fresh red blood in vomit is suggestive of what process?

Back 530

Acute upper GI bleed (e.g. esophageal varix rupture, Mallory-Weiss tear), most likely proximal to the stomach

Front 531

Melena occurs when the bleed is where in the GI tract?

Back 531

Proximal to the ileum

Front 532

Describe melena. This may be mistaken for what condition? How do you tell them apart?

Back 532

Black, tarry, shiny, foul-smelling stools
Iron supplementation → black stools, but NOT tarry or shiny

Front 533

What is the most common cause of iron deficiency anemia?

Back 533

Chronic occult GI bleeding

Front 534

What is "tilt" orthostatic hypotension? What does it indicate?

Back 534

Quickened pulse, falling BP on standing
10% blood loss

Front 535

What is supine hypotension? What does it indicate?

Back 535

Tachycardia, BP < 100 mmHg
25% blood loss

Front 536

Skin and oral cavity telangiectasia + GI bleed incidate what condition?

Back 536

Osler-Weber-Rendu disease (Hereditary hemorrhagic telangiectasia)

Front 537

BUN/Cr > 30 implies what? Why?

Back 537

Upper GI bleed
Creates pre-renal situation

Front 538

What is an anoproctoscopy? What is it helpful to determine?

Back 538

Endoscopy of anal cavity, rectum, and maybe sigmoid colon
Determine whether lower GI bleed is hemorrhoidal

Front 539

When is colonoscopy helpful in evaluating a GI bleed?

Back 539

When bleeding is not brisk and there is sufficient time for colonic prep

Front 540

A patient presents with hematochezia with a blood loss rate of 0.7 ml/min. Hemorrhoidal bleeding is eliminated by anoproctoscopy. What should your next test be? What is the goal of this test?

Back 540

Selective arteriography; localize site of bleed

Front 541

A patient presents with hematochezia with a blood loss rate of 0.2 ml/min. Hemorrhoidal bleeding is eliminated by anoproctoscopy. What should your next test be? What is the goal of this test?

Back 541

Tc99 radionuclide scanning; localize site of bleed

Front 542

Differentiate among visceral, somatic, and referred pain.

Back 542

Visceral: dull, diffuse, and midline
Somatic: sharp, well-localized, lateralized
Referred: well-localized, but in an area remote to dz organ

Front 543

Name six organs (or regions of organs) whose visceral pain localizes to the mid-epigastrum.

Back 543

Stomach, liver, biliary system, pancreas, spleen, duodenum

Front 544

Name five organs (or regions of organs) whose visceral pain localizes to the periumbilical region.

Back 544

Jejunum, ileum, appendix, ascending colon, proximal ~1/3 of transverse colon

Front 545

Name three organs (or regions of organs) whose visceral pain localizes to the suprapubic region.

Back 545

Distal ~2/3 of transverse colon, descending colon, sigmoid colon

Front 546

What two actions may aggravate somatic pain, but will likely not change visceral or referred pain?

Back 546

Coughing, movement

Front 547

What stimulates visceral pain fibers in the gut? In solid organs?

Back 547

Gut and solid organs: distention
Gut: traction, torsion

Front 548

In the abdomen, how does somatic pain occur?

Back 548

Direct stimulation of parietal peritoneum by physical irritants

Front 549

Describe the etiology of referred pain.

Back 549

Visceral afferent neurons linking up at same 2nd order neuron with somatic afferent neurons at a distant (referred) site

Front 550

What are three descriptive terms frequently used for visceral pain?

Back 550

Gnawing, burning, cramping

Front 551

What are two conditions with visceral substernal pain?

Back 551

Heartburn (GERD → pyrosis); acute MI (transient, crushing)

Front 552

Name three conditions classically exhibiting epigastric visceral pain.

Back 552

Pancreatitis, biliary colic (passage of gallstone), non-perforated peptic ulcer

Front 553

How does movement affect visceral pain? Somatic pain? Referred pain?

Back 553

Relieves visceral pain; worsens somatic pain; no effect or relief on referred pain

Front 554

Name three conditions classically exhibiting periumbilical visceral pain.

Back 554

Small bowel obstruction; ischemic colitis; early appendicitis

Front 555

Name three conditions classically exhibiting suprapubic visceral pain.

Back 555

Large bowel obstruction; ischemic colitis; IBS

Front 556

Differentiate colicky and crampy pain. Give two examples of colicky pain and one of crampy pain.

Back 556

Colic: waves of pain (pain → painless → pain → painless) due to peristaltic motion; total small bowel obstruction and kidney stone passage
Cramps: constant pain; bile duct obstruction (biliary colic is a misnomer!!)

Front 557

60yo man c/o dull progressive epigastric pain with radiation to the back, n/v worse with eating/drinking. 3 mo hx of severe RUQ pain with nausea. Dx.

Back 557

Pancreatitis 2/2 gallstone obstruction
RUQ pain likely cholecystitis

Front 558

Name four stimuli that can cause somatic pain.

Back 558

Chemical irritant; inflammation; ischemia; friction against parietal peritoneum

Front 559

Give the likeliest cause of sharp, well-localized mid-epigastric pain.

Back 559

Perforated peptic ulcer

Front 560

Name two possible causes of sharp, well-localized RUQ pain.

Back 560

Cholecystitis; cholangitis

Front 561

Give the likeliest cause of sharp, well-localized LUQ pain.

Back 561

Ischemic colitis at splenic flexure

Front 562

Give the likeliest cause of sharp, well-localized RLQ pain.

Back 562

Late acute appendicits

Front 563

Give the likeliest cause of sharp, well-localized LLQ pain.

Back 563

Acute sigmoid diverticulitis

Front 564

60 yo man c/o fever and LLQ abdominal discomfort. He denies bloody diarrhea. WBC count is elevated. Dx.

Back 564

Diverticulitis

Front 565

30 yo man with hx of PUD c/o sudden onset severe upper mid-abdominal pain, worse with movement. Dx.

Back 565

Perforated peptic ulcer

Front 566

Referred pain to the right scapula is classic for __.

Back 566

Cholecystitis

Front 567

Referred pain to the left shoulder is classic for __ or __.

Back 567

acute MI; GERD

Front 568

Referred pain to the upper neck/shoulder (innervated by C3-5) is classic for __.

Back 568

Perforated peptic ulcer

Front 569

Referred pain to the mid-back is classic for __.

Back 569

Pancreatitis

Front 570

Referred pain lateralized in the inguinal groin is classic for __.

Back 570

a ureteral stone

Front 571

What is a functional bowel dz? Give three examples.

Back 571

Manifestations of GI Sx without organic pathology
Non-ulcer dyspepsia; irritable bowel syndrome; gas Sx

Front 572

What are the six steps in treating IBS?

Back 572

Elicit sx; elicit relationship of sx to stress (but NOT explicitly!); r/o organic dz; make the dx; explain sx; reassure pt

Front 573

You should not treat IBS patients with __ or __. Why not?

Back 573

Laxatives (for painful constipation): can lead to dependency
Anti-diarrheal (for painless diarrhea): can worsen IBS Sx

Front 574

Give the epidemiological profile of a patient with IBS.

Back 574

White Jewish woman in her 20s. If I were Jewish, this would be me.

Front 575

Give three Hx, three PE, and three lab findings which would rule out IBS.

Back 575

Hx: weight loss, hematochezia, onset at age > 50
PE: abdominal mass, LAD, hepatosplenomegaly
Labs: anemia, elevated erythrocyte sedimentation rate, +ve stool guaiac

Front 576

What are the two gases you really need to worry about in the GI tract? When? Why?

Back 576

H2 and CH4; surgery, colonoscopy, and any electrocautery; they are flammable and might explode

Front 577

What is the most common GI Sx?

Back 577

Abdominal bloating

Front 578

What is the gas elimination diet?

Back 578

1 week without milk, 2 days of over-indulgence. If Sx are not cured → 1 week without bread, 2 days of over-indulgence. If Sx are not cured → 1 week without veggies, 2 days of over-indulgence

Front 579

What are two causes of increased flatus?

Back 579

Increased colonic bacterial digestion of undigested food
Increased swallowing of air (high N2)

Front 580

What is the blood supply of the pancreas?

Back 580

Head & uncinate process: gastroduodenal a., SMA
Tail & body: splenic a.

Front 581

Which pancreatic enzymes are secreted in their active forms?

Back 581

Amylase and lipase

Front 582

What cells are present in the endocrine pancreas? What does each one secrete?

Back 582

Alpha: glucagon
Beta: insulin
Delta: somatostatin
G: gastrin
PP: pancreatic polypeptide
D1: vasoactive intestinal polypeptide (VIP)
Enterochromaffin (EC): serotonin (5HT)

Front 583

Give three causes of acute pancreatitis.

Back 583

Obstruction of common bile duct; obstruction of pancreatic duct; alcoholism

Front 584

What are the clinical manifestations of acute pancreatitis?

Back 584

Sudden, severe epigastric pain radiating to back with elevated serum amylase (day 1) and pancreatic lipase (day 3) levels

Front 585

How do you diagnose acute pancreatitis?

Back 585

U/S (visualize biliary tract obstruction), CT/MRI (visualize tumor), ERCP/MRCP (visualize pancreatic duct issues)

Front 586

Give two causes of chronic pancreatitis.

Back 586

Chronic alcoholism; CFTR mutation (but NOT cystic fibrosis!)

Front 587

What is a pancreatic pseudocyst?

Back 587

Area of central hemorrhagic fat tissue surrounded by granulation or fibrous tissue but NOT epithelial cell lining!

Front 588

Name four possible complications of acute pancreatitis.

Back 588

Pancreatic abscess 2/2 infxn; peritonitis (→ fat necrosis); shock and multi-organ failure; pseudocyst formation

Front 589

Name four pathologic changes seen in acute pancreatitis.

Back 589

Acute inflammatory infiltrate + edema
Fat necrosis & saponification (2/2 lipase activity)
Proteolytic auto-digestion (2/2 protease activity)
Hemorrhage (2/2 elastase activity)

Front 590

Name four pathologic changes seen in chronic pancreatitis.

Back 590

Fibrosis & calcification
Exocrine acinar atrophy
Destruction of the isles of Langerhans
± Chronic inflammatory infiltrate

Front 591

Name four benign neoplasms of the exocrine pancreas.

Back 591

Serous cystadenoma; mucinous cystadenoma; solid pseudopapillary tumor; intraductal mucinous tumor

Front 592

What is a precursor lesion to pancreatic adenoCa?

Back 592

Pancreatic intraepithelial neoplasia

Front 593

What epidemiologic factor has the strongest association with pancreatic adenoCa?

Back 593

SMOKING

Front 594

Name four genetic mutations that can lead to pancreatic adenoCa.

Back 594

p53, SMAD4, P16 (all LOF); K-RAS (GOF)

Front 595

What are three clinical manifestations of pancreatic adenoCa in the head of the pancreas?

Back 595

Painless obstructive jaundice; palpable gallbladder; weight loss

Front 596

What are three clinical manifestations of pancreatic adenoCa in the tail of the pancreas?

Back 596

Abdominal pain radiating to back; weight loss; Trousseau's sign (migratory thrombophlebitis)

Front 597

Which portends a more favorable prognosis: painful obstructive jaundice or painless obstructive jaundice? Why?

Back 597

PAINFUL. Gallstone obstructing bile duct, rather than adenoCa of pancreatic head

Front 598

What is the typical presentation of adenoCa of the ampulla of Vater or common bile duct?

Back 598

Jaundice, distended gallbladder

Front 599

Which has a better prognosis: pancreatic adenoCa or pancreatic carcinoid tumor?

Back 599

Pancreatic carcinoid tumor (neoplasms of endocrine pancreas)

Front 600

Pancreatic adenoCa frequently invades what structure within the pancreas itself?

Back 600

Perineurium

Front 601

What is an insulinoma?

Back 601

Insulin-producing neuroendocrine tumor

Front 602

What is Whipple's triad? With what disease is it associated?

Back 602

Insulinoma
- Hypoglycemia
- Anxiety/cold sweat/confusion/stupor/LOC
- Fasting/exercise → attacks; attacks relieved with sugar

Front 603

How can you get CNS Sx from acute liver disease?

Back 603

Elevated blood ammonia

Front 604

Describe the two patterns of focal liver injury.

Back 604

Apoptosis: Councilman or acidophil bodies, no inflammation
Hepatocytolysis: lytic necrosis with inflammation

Front 605

What is the difference between focal and zonal necrosis in liver injury?

Back 605

Focal: scattered injury; may be apoptotic or necrotic/lytic
Zonal: necrosis is confined to one specific zone of liver lobule

Front 606

What is the difference between submassive and massive liver damage?

Back 606

Submassive: involves entire lobule, but not entire liver
Massive: involves entire liver

Front 607

Interface or piecemeal necrosis is typical of what condition(s)?

Back 607

Viral hepatitis (yellow fever), autoimmune hepatitis, steatohepatitis

Front 608

Describe interface hepatitis.

Back 608

Necrosis of the limiting plate (hepatocytes surround the portal triad)

Front 609

Describe bridging necrosis.

Back 609

Necrosis of the hepatocytes bridging between the central venule and the portal triad

Front 610

Describe ballooning degeneration. It is typical in what condition?

Back 610

Swollen edematous hepatocytes; acute hepatitis

Front 611

Describe feathery degeneration. It is typical in what condition?

Back 611

Diffuse foamy swollen hepatocytes; chronic cholestasis

Front 612

In what condition do you typically see Kupffer cell proliferation?

Back 612

Viral hepatitis

Front 613

Define cholestasis. What are the two basic etiologies?

Back 613

Decreased bile secretion to GI tract + increased bile contents in blood
Intrahepatic or extrahepatic obstruction

Front 614

Give three histological manifestations of cholestasis.

Back 614

Canalicular cholestasis; feathery hepatocyte degeneration; cholangiolar proliferation

Front 615

What two subdivisions of intrahepatic obstruction may cause cholestasis? Give two examples of each.

Back 615

Hepatocellular dysfunction: hepatitis, drugs
Small duct obstruction: cirrhosis, primary biliary cirrhosis

Front 616

Give four examples of extrahepatic obstruction that may cause cholestasis.

Back 616

Common bile duct stricture, gallstones, head of the pancreas adenoCa, primary sclerosing cholangitis

Front 617

Name three benign neoplasms of the liver. Which is the most common?

Back 617

Focal nodular hyperplasia; hepatic adenoma; hemangioma
Hemangioma is most common

Front 618

What epidemiologic group is most at risk for focal nodular hyperplasia and hepatic adenoma?

Back 618

Young women of childbearing age

Front 619

What benign liver neoplasm has an association with oral contraception?

Back 619

hepatic adenoma

Front 620

What is the pathologic presentation of focal nodular hyperplasia?

Back 620

Solid mass with a central "stellate" scar
Hepatocytes with bile ducts
Asymptomatic - typically an incidental finding

Front 621

What is the pathologic presentation of hepatic adenoma?

Back 621

Solid mass; NO central scar!
Hepatocyte proliferation with NO bile ducts

Front 622

What is the major risk of hepatic adenoma? Is this risk present in focal nodular hyperplasia?

Back 622

Rupture (50-60% of cases) → hemoperitoneum
ONLY risk of adenoma - not of focal nodular hyperplasia!

Front 623

What is the major risk of hepatic hemangioma?

Back 623

Bleeding and thrombocytopenia

Front 624

Name seven epidemiologic associations with hepatocellular carcinoma.

Back 624

HBV, HCV, EtOH, cirrhosing metabolic disorders, aflatoxin, androgen, G6PD deficiency

Front 625

Name five metabolic disorders that may predispose a person to hepatocellular carcinoma. Why is one of these not like the others?

Back 625

Hemochromatosis, A1AT deficiency, Wilson's disease, tyrosinemia (cirrhotic conditions)
G6PD deficiency (non-cirrhotic!)

Front 626

What causes aflatoxin? How does it predispose to hepatocellular carcinoma?

Back 626

Aspergillus
Creates a point mutation in p53

Front 627

Name four ways fibrolamellar carcinoma differs from hepatocellular carcinoma.

Back 627

Better prognosis
Presents in children (rather than primarily in adults)
No association with HBV
No association with cirrhosis

Front 628

Describe the pathologic appearance of fibrolamellar carcinoma.

Back 628

Large cells with pink cytoplasm
Lamellar collagen deposition
On CT: liver mass with central scarring
Elevated AFP

Front 629

Name six associations with cholangiocarcinoma. What two things are notably NOT associated with development of cholangiocarcinoma?

Back 629

Primary sclerosing cholangitis; hepatolithiasis; parasites (liver fluke); thorotrast (iatrogenic); cystic dilation of bile ducts
NOT associated with: cirrhosis, HBV

Front 630

What is primary sclerosing cholangitis?

Back 630

p-ANCA mediated autoimmunity against the bile ducts
Most cases occur in those with ulcerative colitis
Risk factor for cholangiocarcinoma

Front 631

How do you diagnose cholangiocarcinoma?

Back 631

Jaundice; mucin positive; AFP negative (no hepatocyte involvement)

Front 632

What is a hepatoblastoma? What is its prevalence?

Back 632

Pediatric neoplasm composed of embryonic epithelial cells
Unusual!

Front 633

When does hepatoblastoma usually present?

Back 633

Before age 2

Front 634

Angiosarcoma is typically associated with what epidemiologic factor? Give four examples.

Back 634

Exposure: thorotrast (radiocontrast from '30s-50s), PVC, arsenic, androgens

Front 635

What is the most common liver neoplasm in the US?

Back 635

Metastasis!!!!!

Front 636

Why is the liver a popular site for metastasis?

Back 636

Like lung, dual blood supply

Front 637

Define acute liver disease.

Back 637

Sudden appearance of clinical or lab features of liver dz in a person with no past evidence of liver dz

Front 638

What is the best test to determine severity of acute liver disease?

Back 638

PT

Front 639

Give five pathologic features of acute viral hepatitis.

Back 639

Balloon degeneration; Kupffer cell proliferation; lymphocytic (NOT PMN) infiltrate; hepatocytolysis a/o apoptosis; portal inflammation

Front 640

Give five viral etiologies of acute liver disease.

Back 640

HAV, HBV, HEV, CMV, EBV

Front 641

Why is HCV not considered a common cause of acute liver disease?

Back 641

Rarely presents acutely! >75% of cases have NO acute Sx, and HCV can NOT cause fulminant hepatic failure

Front 642

Name four toxic causes of acute liver disease. Which one is epidemiologically constrained?

Back 642

EtOH, acetaminophen, isoniazid, aspirin (in kids → Reye's sd)

Front 643

What are the clinical manifestations of acute icteric hepatitis?

Back 643

Prodromal phase: anorexia, nausea, vomiting
Icteric phase: pruritic jaundice
Recovery phase: return of appetite, gradual loss of jaundice

Front 644

Define asymptomatic hepatitis.

Back 644

Abnormal LFTs without clinical sx

Front 645

What is the treatment for autoimmune acute hepatitis?

Back 645

Glucocorticoids

Front 646

How do you treat acute hepatitis? What is the one exception?

Back 646

Watchful waiting (usually self-resolving) except in autoimmune → tx with glucocorticoids (prednisone)

Front 647

What are three indications for hospitalization in acute liver disease?

Back 647

Severe dehydration; bile duct obstruction (jaundice, fever, RUQ pain); encephalopathy (fulminant hepatic failure)

Front 648

What are the stages of fulminant hepatic failure?

Back 648

Change in sleep pattern → drowsiness and AMS → unconscious but arousable → unarousable

Front 649

Define fulminant hepatic failure.

Back 649

Development of mental sx within 6 weeks of acute hepatitis onset with no prior evidence of liver dz

Front 650

What are three signs that indicate a poor prognosis of fulminant hepatic failure?

Back 650

Worsening mental status; persistent hypoglycemia; rising PT

Front 651

How do you treat fulminant hepatic failure?

Back 651

Acetylcysteine (if acetaminophen toxicity)
Prednisone (if autoimmune liver dz)

Front 652

What is the only DNA hepatitis virus?

Back 652

HBV

Front 653

What is the only hepatitis virus which depends on another?

Back 653

HDV (requires presence of HBV)

Front 654

Simultaneous HBV and HDV infection results in what short- and long-term pathologies?

Back 654

Short: acute fulminant hepatitis (→ recovery or death)
Long: chronic hepatitis → cirrhosis

Front 655

A patient with chronic HBV infection has developed a "new" bout of hepatitis. What do you suspect?

Back 655

HDV infection

Front 656

What non-hepatic complications are frequently associated with HBV infection?

Back 656

Polyarteritis nodosa; membranous GN; cryoglobulinemia

Front 657

Interpret this HBV panel:
- HBsAg negative
- anti-HBc negative
- anti-HBs negative

Back 657

Susceptible

Front 658

Interpret this HBV panel:
- HBsAg negative
- anti-HBc negative
- anti-HBs positive

Back 658

Immune due to vaccination

Front 659

Interpret this HBV panel:
- HBsAg negative
- anti-HBc positive
- anti-HBs positive

Back 659

Immune due to past infection (cleared)

Front 660

Interpret this HBV panel:
- HBsAg positive
- anti-HBc positive
- IgM anti-HBc positive
- anti-HBs negative

Back 660

Active acute infection

Front 661

Interpret this HBV panel:
- HBsAg positive
- anti-HBc positive
- IgM anti-HBc negative
- anti-HBs negative

Back 661

Active chronic infection

Front 662

What does the presence of HBeAg indicate? What is another indicator of the same thing?

Back 662

High degree of HBV infectivity; HBV DNA is also closely correlated with infectivity

Front 663

HEV is most dangerous in what group?

Back 663

Pregnant women

Front 664

In which forms of hepatitis does Ab confer protective immunity?

Back 664

HAV, HEV, HBV (but ONLY anti-HBs)

Front 665

Define chronic liver disease.

Back 665

Clinical or lab evidence of liver dz for > 6 months

Front 666

What are the three general causes of chronic liver disease?

Back 666

Hepatocellular; cholestasis; venous outflow obstruction

Front 667

Describe the symptoms of decompensated liver dz.

Back 667

Edema/ascites; spontaneous bacterial peritonitis; portal HTN; hepatic encephalopathy; hepatorenal Sd

Front 668

What is Budd-Chiari syndrome?

Back 668

Occlusion of the hepatic veins (→ abdominal pain, ascites, hepatomegaly)

Front 669

What are the three general causes of portal HTN? Give two examples of each.

Back 669

Pre-hepatic: portal vein thrombosis, splenic vein thrombosis
Hepatic: liver cirrhosis, tumor
Post-hepatic: CHF, hepatic vein occlusion (→ Budd-Chiari)

Front 670

What effect of portal HTN may lead to devastating acute clinical consequences?

Back 670

Esophageal variceal bleeding

Front 671

How do you treat variceal bleeding?

Back 671

Somatostatin, beta blockers, endoscopic surgery

Front 672

What are the three causes of ascites?

Back 672

Decreased oncotic pressure (2/2 ↓ albumin production)
Increased hydrostatic pressure (2/2 portal HTN)
Increased intravascular volume (2/2 salt retention)

Front 673

What is SAAG? What does it help differentiate?

Back 673

Serum-ascitic albumin gradient; determines whether ascites is due to portal HTN or any other cause

Front 674

A high SAAG indicates liver disease due to __. How do you differentiate within this category?

Back 674

Portal HTN
- high protein: congestive heart failure
- low protein: cirrhosis

Front 675

A low SAAG indicates liver disease due to __. How do you differentiate?

Back 675

Infection or malignancy
High WBC count in ascites: infectious etiology
High RBC count in ascites: malignant

Front 676

What is the treatment for ascites? What determines its efficacy?

Back 676

Salt restriction & diuretics
Most useful in high SAAG conditions

Front 677

Define spontaneous bacterial peritonitis.

Back 677

Primary ascites without apparent intra-abdominal cause

Front 678

What defines bacterial peritonitis in ascites?

Back 678

PMN count > 250/μL and bacterial culture

Front 679

What is the most common bug in spontaneous bacterial peritonitis?

Back 679

E. coli

Front 680

What are the clinical manifestations of spontaneous bacterial peritonitis?

Back 680

Abdominal pain; fever; ileus; shock; rebound tenderness

Front 681

How do you treat spontaneous bacterial peritonitis?

Back 681

IV cefotaxime

Front 682

How do you diagnose hepatic encephalopathy?

Back 682

Increased serum [NH3]; apraxia

Front 683

Name three clinical manifestations of hepatic encephalopathy.

Back 683

LOC, coma, asterixis

Front 684

Give three treatments for hepatic encephalopathy.

Back 684

Treatment of underlying cause; ↓ protein intake; lactulose

Front 685

Define hepatorenal syndrome.

Back 685

Progressive renal failure in pt with chronic liver dz

Front 686

How do you treat hepatorenal syndrome?

Back 686

Liver transplant

Front 687

What is the cause of primary biliary cirrhosis?

Back 687

Anti-mitochondrial Ab

Front 688

AST>ALT in what circumstance? Why?

Back 688

Alcohol use! (→ hepatitis, steatosis, cirrhosis); mitochondrial damage due to EtOH