GI Deck 1 Flashcards
1
Q
What is the distance between the incisors to the stomach?
A
40 cm
2
Q
What is the position of the esophagus in the thoracic cavity?
A
posterior
3
Q
What muscles make up the upper esophageal sphincter?
A
Lower fibers of inferior pharyngeal constrictor
Cricopharyngeus
4
Q
What is the state of the upper esophageal sphincter at rest?
A
Tonically closed
Relaxes during a swallow
5
Q
What occurs during the oral phase of swallowing?
A
Bolus propelled back by tongue
Tongue squeezes against palate (anterior ot posterior)
This is voluntary
6
Q
What occurs during the pharyngeal phase of swallowing?
A
Soft palate elevates to close off nasopharynx
Larynx moves anterio-superiorly to bring larynx away from path of bolus and open the UES
Larynx closes and UES relaxes, and the bolus is propelled into the esophageal inlet by pharyngeal muscles
This is involuntary
7
Q
Is the LES a true sphincter?
A
No - it is a high pressure zone
8
Q
What structure helps the LES maintain its tone?
A
The diaphragm - the LES itself has some muscle tone, but the diaphragm really provides the pressure.
9
Q
What neural factors increase LES pressure?
A
Cholinergics
α- adrenergic agonists
β-adrenergic blockers
10
Q
What hormones can increase LES pressure?
A
Gastrin
Motilin
Substance P
11
Q
What food can increase LES pressure?
A
Protein
12
Q
What drugs can increase LES pressure?
A
Pro-kinetics (metoclopramide, doperidone)
Histamine
Antacids
13
Q
What neural factors decrease LES pressure?
A
Cholinergic antagonists
α adrenergic blockers
β- adrenergic agonists
Nitric oxide
14
Q
What hormones can decrease LES pressure?
A
Secretin
CCK
Somatostatin
Progesterone (e.g. pregnancy)
15
Q
What foods can decrease LES pressure?
A
Fats
Chocolate
Ethanol
Peppermint
16
Q
What drugs can decrease LES pressure?
A
Theophylline
Ca- channel blockers
Morphine
Diazepam
Serotonin
17
Q
What are some symptoms of esophageal disorder?
A
Dysphagia
Heartburn
Odynophagia (pain on swallowing)
Chest pain
Regurgitation
Atypical (hoarseness, cough, wheeze, sore throat)
18
Q
What is dysphagia??
A
Sense of impaired transport of bolus through esophagus
19
Q
What is pyrosis?
A
Heartburn
Substernal burning
Due to reflux of gastc contents (acid, bile)
Occurs after meals, worse with bending, relieved with antacids
20
Q
What is odynophagia?
A
Pain on swallowing
21
Q
What does the chest pain of esophageal disorder typically mimic?
A
Angina pectoris
22
Q
What is regurgitation with respect to esophageal disorder?
A
Entry of gastric contents inot esophagus or mouth
23
Q
What does a barium esophagram tell you?
A
Evaluates a structural lesion (stricture, web, hiatal hernia)
Can sometimes demonstrate GE reflux
24
Q
What does an endoscopy with biopsy of the esophagus tell you?
A
Directly visualizes esophageal mucosa
Enables tissue diagnosis
25
What does endoscopic ultrasound (esophageal) tell you?
Useful for imaging lesions that are in esophageal wall or immediately adjacent to esophagus
Fine needle aspirate is possible
26
What do we see here?
Esophageal cancer
27
What is esophageal monometry useful for?
Measures pressures, contractile activity and sphincter function
Useful for motility disorders
Can demonstrate tendency for GE reflux
28
What do acid reflux (pH) studies tell you?
Measures esophageal pH
24-hour pH probe
Quantitates teh amount and duration of reflux
Can correlate with symptoms
29
What is GERD?
Gasroesophageal refulx disease
Casued by reflux of gastric contents into the esophagus
Not all reflux causes disease (not all reflux is acid)
30
What causes GERD?
Reflux of gastric contents into esophagus
31
What are symptoms of GERD?
Heartburn (worse with food, lying supine, better with antacids)
Chest pain, dysphagia, hoarseness
32
What are key diagnostic tests for identifying GERD?
History
24-hour pH monitoring (reflux itself)
Endoscopy for the effects of reflux
LES pressure and barium swallow for the potential to reflux
33
What are the aggressive pathogenic factors of GERD?
Acid (or bile)
34
What are defensive pathogenic factors of GERD?
Anti-reflux barrier (LES and crural diaphragm)
Esophageal acid clearance (saliva, esophageal peristalsis, gastric emptying, intact esophageal mucosa, hiatal hernia)
35
What is the most important defensive factor against the development of GERD?
Anti-reflux barrier
LES and Crural diaphragm
36
What are issues with esophageal acid clearance that can lead to GERD?
Reduced saliva production
Malfunctioning esophageal peristalsis
Faulty gastric emptying
Non-intact esophageal mucosa
Hiatal hernia --\> more acid in the esophagus --\> GERD (thanks SFong!)
37
What do we see here?
GERD
38
What is a hiatal hernia?
Increase in transient LES relaxations (TLESRs)
Acid pocket within proximal stomach
Loss of crural pinch at the GE junction
39
What are the two types of hiatal hernias?
Sliding and para-esophageal
40
What is this?
Sliding hiatal hernia
41
What is this?
Para-esophageal hiatal hernia
42
What test do you perform to demonstrate increased acid exposure?
24-hr pH
43
What test do you do to correlate acid exposure to symptoms in GERD?
24-hr pH
44
What test do you perfrom to show evidence of mucosal disease in GERD?
Endoscopy
45
What test do you perform to identify the mechanisms of reflux in GERD?
Esophagram or manometry
46
What are complications of GERD?
Mucosal ingury (esophagitis, ulcer)
Stricture
Barret's metaplasia (squamous epithelium changes to columnar epithelium - premalignant)
Esophageal adenocarcinoma
47
What algorithm do you follow to identify the cause of dysphagia?
48
What is the first question you ask a patient with dysphagia??
Solids or liquids?
49
What test can you use to identify a mechanical vs a motor disorder of dysphagia?
Structural first (endoscopy or barium swallow)
Followed by esophageal manometry
50
What is achalasia?
Failure of smooth muscle fibers to relax, which can cause a sphincter to remain closed and fail to open when needed (LES)
51
What ist he pathogenesis of achalasia?
Loss of inhibitory ganglion cells within myenteric plexus
LES remains tonically contracted
52
What are abnormalities seen on manometry in achalasia?
Hypertensive LES
Impaired LES relaxation
Aperistalsis of body of esophagus
53
What are clinical symptoms of achalasia?
Dysphagia
Regurgitation
Eventual weight loss
Chest pain
54
What od we see here?
Achalasia
55
What do we see on the right?
Achalasia
56
How do you treat achalasia?
Botulinum toxin
Pneumonic dilation
Heller myotomy
57
What diseases cause pseudo-achalasia?
Chagas' disease (trypanosma cruzii infection)
Cancer of GE junction (more rapid onset, more weight loss)
58
What do you see on barium swallow in scleroderma?
Loss of LES function (GE reflux)
59
What do you see in manometry in scleroderma?
Poor esophageal motility
Low LES pressure
60
What is diffuse esophageal spasm?
Condition in which uncoordinated contractions of the esophagus occur. It is thought to result from motility disorders of the esophagus. These spasms do not propel food effectively to the stomach. It can cause dysphagia, regurgitation and chest pain.
61
What are symptoms of diffuse esophageal spasm?
Chest pain, odynophagia or both
May mimic angina pectoris
On X-ray you can see corkscrew esophagus
62
What is this?
Diffuse esophageal spasm (corkscrew esophagus)
63
What do you see on manometry in diffuse esophageal spasm?
Simultaneous contractions
Repetitive contractions
LES usually normal
64
What do we see on the right?
Diffuse esophageal spasm
65
How do you treat diffuse esophageal spasm?
Muscle relaxants
Calcium-channel blockers
Nitrates
Rarely surgery
66
What is nutcracker esophagus?
Disorder of the movement of the esophagus, and is one of many motility disorders of the esophagus, including achalasia and diffuse esophageal spasm. It causes difficulty swallowing, or dysphagia, to both solid and liquid foods, and can cause chest pain; it may also be asymptomatic
Very high amplitude contractions (on manometry)
Normal peristalsis and LES
67
What esophageal disease on manometry has normal amplitude contractions with abnromal contraction frequencies?
Diffuse esophageal spasm
68
What esophageal disease has abnormal amplitude contractions (high) with normal peristalsis and LES?
Nutcracker esophagus
69
What are features of manometry of nutcracker esophagus?
High amplitude contractions
Normal peristalsis and LES
70
What do we see on the right?
Nutcracker esophagus
71
What part of the GI is this?
Esophagus
72
Identify the mucosa
73
Identify the salivary duct 
74
Identify the muscularis mucosae, submucosa 
75
Identify a mucous salivary gland
76
Identify the muscularis propria
77
Identify the smooth muscle
78
Identify the myenteric plexus 
79
Identify the skeletal muscle 
80
Which part of the esophagus do you have skeletal muscle?
Proximal (upper 1/3)
Distal esophagus only has smooth muscle
81
Where do new squamous cells in the esophagus come from?
Stem cells - basal cells - mature cells
These then flatten and desquamate at sufrace
82
What is the "Z" line?
Line between stomach and esophagus
esophagus = lighter/shinier
stomach = pinker
83
What can cause chemical esophagitis?
Injury and complications due to household and gardening chemicals, etc
Nature of injury depends on chemical
84
What is significant about alkalies with respect to chemical esophagitis?
Can be odorless and tasteless and can cause rapid injury
They are especially dangerous
Can cause necrosis, saponification, perforation and death
85
What are some long-term complications of chemical esophagitis?
Chronic ulcer, scarring, stricture and eventually squamous cell carcinoma
86
Why can pills cause damage to esophagus?
Pill sticks to mucosa - causes prolonged contact with mucosa
Perhaps during sleep - pill becomes sandwiched in collapsed esophagus
87
What do you see on endoscopy that is characteristic of esophagitis due to pills?
"Kissing ulcers"
88
Why do pills commonly cause damage to an esophagus during sleep?
Pill becomes sandwiched in collapsed esophagus, there are no secretions swallowign or peristalsis, so it can cause injury
89
What does esophagitis due to pills feel like/present like?
Acute chest pain
It is self-limited though
90
What is particular about the esophagitis that is caused by bisphosphanates?
Reacts to produce corrosive compound in stomach.. If any regurgitation/reflux, it will damage the distal esophagus
91
What is the most common infectious esophagitis?
Candida esophagitis
Immunocompromised (but not always)
92
What are signs and symptoms of candida esophatitis?
Odynophagia (painful swallowing)
Oral thrush
93
What do you find on endoscopy of candida esophagitis?
Whitish plaques, desquamated cells and fungi
Stains
94
Which patients get CMV esophagitis?
Exclusively immunocompromised patients
Indicative of viremia (you don't get local infection)
95
Which cells of the esophagus does CMV infect?
Mesenchymal cells (endothelium, fibroblasts, myocytes)
Does NOT infect squamous cells
96
What is this?
Cytomegalic endothelial cells due to cytomegalovirus (CMV)
CMV esophagitis
97
Who does herpers esophagitis affect?
Immunocompetent or immunocompromised hosts
98
What cells does herpes esophagitis affect?
Squamous cells
99
What occurs pathologically in herpes esophagitis?
Cell-cell detachment
Multinucleation
"Ground glass" nuclei
100
What do we see here?
**Herpes esophagitis**
Cell-cell detachment
Multinucleation
"Ground glass" nuclei
101
What area of the esophagus do you want to take a biopsy if you suspect CMV or herpes esophagitis?
The border between ulcerated and intact esophagus epithelium
102
What are some risk factors for reflux esophagitis?
LES inocmpetence
High abdominal pressure
Reduced saliva
Other (bulimia, NG intubation)
103
What causes reflux esophagitis?
Injury due to gastric acid, pepsin and duodenal contents (trypsin, bile)
104
What area of the esophagus is most affected by reflux esophagitis?
Distal
105
What do we see here?
GERD
Congested capillaries
106
What do you see in reflux esophagitis on histology?
Edema (wide intracellular spaces)
Ballooned squamous cells
Basal cells hyperplasia
Eosinophils
Congested capillaries
107
What do you see here? 
Reflux esophagitis
Edema
Balloooned squamous cells
Basal cell hyperplasia
Eosinophils
108
What do you see here?
Ulcer exudate
Reflux-associated (peptic) ulcer
109
What are complications of esophageal ulcers?
Scarring and stricture (dysphagia)
Regeneration and development of Barrett esophagus
During ulcer - odynophagia, hematemesis (vomit blood)
110
What is eosinophilic esophagitis?
2nd most common esophagitis (and rising)
Dysphagia and food impaction
Antigen driven - 75% have allergic overlay
Treated with dietary restriction, steroids
111
What type of esophagitis has an allergic component?
Eosinophilic esophagitis
(treated as such - restriction of antigen (diet) or steroids)
112
What is this?
Eosinophilic esophagitis
Transverse rings (trachealization)
Longitudinal furrows
Tiny white mucosal plaques
113
What is this?
 
Eosinophilic esophagitis
Note the eosinophil aggregates near surface and the fibrosis at base
114
How do you distinguish eosinophilic esophagitis from GERD with respect to age of patient?
EoE - children and adults
GERD = adults usually
115
How do you distinguish eosinophilic esophagitis from GERD with respect to symptoms
EoE = dysphagia, food impaction
GERD = heartburn
116
How do you distinguish eosinophilic esophagitis from GERD with respect to etiology
EoE = food and airborne allergens
GERD = gastroduodenal reflux
117
How do you distinguish eosinophilic esophagitis from GERD with respect to pathogenesis?
EoE = IgE and cell mediated injury
GERD = chemical
118
How do you distinguish eosinophilic esophagitis from GERD with respect to site of injury?
EoE = pan-esophageal
GERD = distal
119
How do you distinguish eosinophilic esophagitis from GERD with respect to therapy?
EoE = food restriciton, steroids
GERD = suppression of acid secretion and reflux
120
What is Barrett esophagus?
Columnar lined esophagus in response to gastroesophageal reflux
A form of metaplasia (replacement of squamous mucosa by columnar)
No symptoms
Risk factor for esophageal adenocarcinoma
seen in 5-15% of GERD patients
121
What are characteristics of Barrett esophagus?
Salmon-colored mucosa
Circumferential, tongues, islands (\<3cm = short-segment Barrett Esophagus)
122
What is this?
Barrett esophagus
123
If this was taken from an esophagus, what do you suspect?
Barrett esophagus - metaplasia
124
What are the steps between Barrett esophagus to adenocarcinoma?
Barrett esophagus -\> low grade -\> high grade -\> cancer
This takes years but patients usually don't know
125
How do you diagnose Barett esophagus?
Endoscopy and biopsies for dysplasia
126
Can you visualize dysplasia of Barett Esophagus endoscopically?
NO - need biopsy
127
How do you manage Barrett esophagus?
Aggressive treatment of GER
Endoscopic surveillance
Ablation or surgery
128
What is the progression seen here in the esophagus?
Barrett esophagus to adenocarcinoma
129
Who is the main group of patients who get Barrett adenocarcinoma?
White males
130
What are risk factors for Barrett adenocarcinoma?
Duration, and lenght of Barrett esophagus
Dysplasia and genetic factors
131
What are symptoms of Barrett adenocarcinoma?
Dysphagia (solids then liquids)
**Weight loss**
132
What is squamous cell carcinoma?
Carcinoma arising directly from the squamous cells of the esophagus
133
What are risk factors for squamous cell carcinoma?
Underdeveloped regions - dietary deficiencies, aflatoxins, indoor coal burning
Industrialized countries - alcohol and smoking (synergistic)
Other - achalasia, lye stricture, celiac disease
134
In the US what demographics get squamous cell carcinoma more commonly?
Males more than females
Age \> 50
Smoking + alcohol history
Urban \> rural environments
Higher incidence in African americans
135
What does it mean if a patient with squamous cell carcinoma present with symptoms?
Advanced disease more commonly
136
What are clinical features of squamous cell carcinoma?
Progressive dysphagia
Weight loss
Hemoptysis, hematemesis
Hoarseness (tumor invasion of recurrent laryngeal nerve)
137
What do you see here?
Squamous cell carcionma - white = squamous cells
138
What is the natural history of squamous cell carcinoma?
Median survival is less than 1 year
5 year survival is 5-10%
Most deaths occur from complications, not metastases
139
What is the cause of mortality in squamous cell carcionmas?
Mostly local complications, not metastases
140
What do you see here?
Squamous cell dysplasia, a precursor of squamosu cell carcinoma
141
What is squamous cell dysplasia?
Precursor to squamous cell carcinoma
142
Where is the cardia of the stomach?
Where esophagus joins the stomach
143
How many layer of muscles does the stomach have?
3
Oblique layer, circular layer, longitudinal layer
These are seperate from muscularis mucosae of the mucosa
144
What are the layers of the stomach?
Mucosa
Submucosa
Muscularis externa
Serosa
145
Where do you find fundic glands?
Proximal stomach
146
Where do you find pyloric glands?
Distal stomach
147
What do parietal cells produce?
Acid (HCl)
Intrinsic factor
148
What do chief cells produce?
Pepsinogen
149
How do parietal and chief cells work together to promote digestion?
Parietal cells produce the acid that helps cleave pepsinogen (produced by chief cells) to pepsin
150
Where are the stem cells in the stomach mucosa found?
Neck cells in a gastric pit
151
What do ECL cells produce?
Histamine
152
What do the foveolar cells produce?
Mucous
153
What are the red cells?
Foveolar
154
What are the yellow cells?
Mucous neck cells
155
What are the green cells?
Parietal cells
156
What are the purple cells?
Chief cells
157
Identify the layers/cells 
158
What is difference between pyloric glands and fundic glands?
Pyloric has G cells (make gastrin)
In the gland part- you see mucous producing cells too
Pyloric in antrum
159
What do G cells make?
Gastrin
160
What are the functions of the stomach?
Mechanical churning of food
Initiates chemical digestion of food
Produces intrinsic factor (for vit B12)
161
How does the stomach initiate the chemical digestion of food?
Acid degrades protein
Pepsin begins protein digestion
Lipase digests fat (minor function)
162
What is the funciton of the fundus and body (proximal portion) of the stomach?
Storage and secretion
163
What is the function of the antrum (distal stomach)?
Mixing and grinding
164
What factors decrease the rate of gastric emptying?
Acid - trigger secretin production, which inhibits emptying
Amino acids and fatty acids - trigger cholecystokinin (CCK), also inhibits emptying
Osmolality - triggers vagal afferents to decrease rate
165
What is the effect of acid in the duodenum?
Triggers secretin production which will feed back and decrease gastric emptying
166
What is the result of amino acids and fatty acids in the duodenum?
trigger cholecystokinin production (CCK) which feeds back and decreases gastric emptying
167
What is the "ileal brake"?
Carbohydrates in the ileum will trigger peptide YY which will result in decreased gastric emptying
168
What effect do carbohydrates in the ileum produce?
Peptide YY production which feeds back to decrease gastric emptying
169
What is motilin?
Pro-kinetic hormone made in the duodenum
Binds to receptors on smooth muscle throughout gut
Increases phase III contractions of migrating motor complex
170
What drug is a motilin agonist?
Erythromycin - produces stomach cramps
171
What GI side effect is common with erythromycin?
Motilin agonist which causes cramps
172
What is one of the most potent stimuli for gastric secretion?
Gastric distention
173
What is the result of gastric distention?
Increased secretions (acid, pepsin, gastrin)
174
What is GRP?
Gastrin releasing peptide
Vagal afferents release GRP which stimulate G cells to release gastrin
This goes on to affect parietal cells to secrete acid
(The vagal afferents are activated in response to gastric distention)
175
What stimulates parietal cells to produce acid/intrinsic factor?
Vagal activity
Gastric distention
Gastrin
Histamine
176
What stimulates chief cells to produce pepsinogen I and II?
Vagal activity
Gastric distention
Gastrin
Histamine
177
Why do parietal cells have evaginations on their apical surface?
To increase surface area to allow for more proton pumps to be able to locate and secrete acid
178
What are the three receptors on a parietal cells?
CCK-B = binds gastrin
H2 = binds histmaine
M3 = binds ACh
179
How do parietal cells secrete acid in result from a stimulus (say from gastrin or histamine)?
Receptor binding causes resting pumps to locate to apical surface and pump out acid
180
Where do G cells live?
antrum of stomach
181
What is the effect of gastrin?
Goes into blood stream, travels throughout body, finds parietal cells in the body/fundus of stomach
Stimulates acid production/secretion
Also affects ECL cells which produce histamine, which also tell parietal cells to secrete acid
182
What is the role of ECL cells in digestion?
Secrete histamine in response to gastrin (from G cells)
Histamine acts on parietal cells to stimulate acid production
183
What is the role of acetylcholine in parietal cell acid control?
Acts directly and indirection (via ECL cells) to increase acid secretion
184
What hormone is secreted by D cells?
somatostatin - turns of G cell gastrin
185
What is the effect of somatostatin on G cells?
Turns off gastrin production
186
What is the "pH meter" of the GI?
D cells - too acidic = turns off signals to produce acid
187
Why doesn't the stomach digest itself?
There is the mucus-bicarbonate layer
188
What is significant of the mucus-bicarbonate layer with respect to disease?
It provides a relatively neutral niche wherein H. pylori can camp out
189
What is the effect of NSAIDs on the mucous-bicarbonate layer?
Inhibits prostaglandin, bicarb and mucus production whcih are crucial for the mucus-bicarbonate layer
So it can allow for the erosion of the stomac mucosa
190
What is gastritis?
superficial erosions of the stomach wall - don't go very deep
191
What are gastric ulcers/how are they different from gastritis?
They go deep - have a whitish exudate over them
192
What is this?
Gastric ulcer
193
What is generally the cause of duodenal ulcers?
Hypersecretion of acid
194
What is generally the cause of gastric ulcers?
Disruption of mucous barrier (NSAIDs, aspirin)
195
What infection can cause duodenal ulcers?
H. pylori
Suppresses D cells which results in acid hypersecretion (via unopposed gastrin)
196
What are hte major causes of peptic ulcer disease?
H. pylori
NSAIDs, aspirin
Stress (due to ischemia) = major burns, or head trauma
Gastrinoma
(rare = systemic mastocytosis causes histamine; basophilic leukemia produces histamine)
197
What is the route of transmission of H. pylori?
Probably fecal-oral early in life
198
What is the only known reservoir of H. pylori infection?
**gastric** mucosa
199
What types of epithelium does H. pylori infect?
Gastric type only
Not intestinal or squamous
200
What is a major effect on the normal mediators of digestion that H. pylori affects?
Inhibits somatostatin by antral D cells = permits increase in gastrin production which promotes acid hypersecretion
201
What is Zollinger-Ellison Syndrome?
Gastrinoma - cells autonomously produce gastrin, all the time
Don't get shut off by normal methods
Can be found in duodenum or in pancreas
202
How do peptic ulcers present?
Pain - epigastric, sometimes relieved by food
Bleeding - occult or overt
Gastric outlet obstruction - in duodenal bulb or pyloric channel
Perforation - peritonitis
Penetration - erosion of ulcer into adjacent organ (pancreas, colon)
203
How are peptic ulcers treated?
Remove inciting agent - treat H. pylori, avoid NSAIDs and other irritants, remove gastrinoma
Pharmacologically - neutralize acid, block acid production, enhance prostaglandin produciton
Surgery - rare, done for complicated PUD (vagotomy, antrectomy, subtotal gastrectomy)
204
What are surgical treatment strategies for peptic ulcer disease?
Vagotomy - but blocks motility
Cut and re-attach (Billroth) antrectomy
205
What is a roux-en-Y anastomosis?
206
What can cause hypergastrinemia?
Insufficient amounts of luminal acid (common) - due to use of PPIs or H2 blockers; Autoimmune destruction of parietal cells (pernicious anemia)
Overproduction of gastrin (rare) - G-cell hyperpasia; retained antrum after surgical antrectomy
Ectopic produciton of gastrin (rare) - gastrinoma
207
What is dangerous about acute erosive gastritis?
Potential for serious bleeding
208
What is the etiology of acute erosive gastritis?
Drugs, especially NSAIDs
Severe physiologic stress (stress ulcers)
209
What are Curling ulcers?
Following burns
210
What are Cushing ulcers?
Following brain trauma or surgery
211
What do we see here?
acute erosive gastritis
212
What is "chemical" gastropathy?
Damage to the stomach that is not inflammatory in nature (that is gastritis)
See erythema on endoscopy
Occurs independently or in the background of erosive gastritis
Mostly due to NSAIDs, bile reflux
213
What do you see here in these gastric pits?
Gastropathy - loss of epithelial mucin; dilated capillaries; "corkscrew" gastric pits
214
When do you see "corkscrew" gastric pits?
Gastropathy (no inflammation)
215
When you see erythema on endoscopy of the stomach, what are you considering?
Gastropathy (will not see inflammation on biopsy)
216
What do you see in these gastric pits?
Chronic gastritis - mucosa infiltarated by mononuclear inflammatory cells and eosinophils
217
What do you see microscopically in chronic gastritis?
218
What is a problematic progression of chronic gastritis?
Atrophic gastritis - atrophy (loss of glands) and/or intestinal metaplasia
219
What do oyu see here?
Atrophic gastritis with intestinal metaplasia
A sequellae of chronic gastritis
220
What part of the stomach does autoimmune gastritis afflict?
Body of the stomach
221
What part of the stomach does H. pylori gastritis afflict?
Antrum
222
What part of the stomach does multifocal atrophic gastritis afflict (MAG)?
Pangastritis (all)
223
What are key features of chronic autoimmune gastritis?
Gastric body only
Loss of parietal cell mass
Hypochlorhydria (low HCl)
B12 deficiency, pernicious anemia - no intrinsic factor
Antral G cell hyperplasia
Hypergastrinemia
ECL cell hyperplasia
Carcinoid tumors (ECL cells proliferating)
Higher risk of cancer, and often have other autoimmune diseases
224
Normal is on the left, what do you see on the right?
Chronic autoimmune gastritis
Reduced glands, loss of parietal and chief cells
Replacement by antral and intestinal epithelium (metaplasia)
Chronic inflammation
225
What are gross features of chronic autoimmune gastritis?
Flat, loss of rugae
226
What do you see here, normal is on the left?
Flat, loss of rugae
Chronic autoimmune gastritis
227
What do you find in laboratory studies of chronic autoimmune gastritis?
Anti-parietal cell and anti-intrinsic factor antibodies
Elevated gastric pH
Elevated serum gastrin
Low vit B12
Megaloblastic anemia
228
What do you see here (this is in the antrum)?
Hyperplastig G cells
IN response to chronic autoimmune gastritis
229
What do you see here?
ECL cell hyperplasia that can be seen from chronic autoimmune gastritis
230
What can you do to make carcinoid tumors regress?
Remove part of the antrum of the stomach - this will allow these carcinoid tumors (typically ECL cell derived) to regress
231
Where does inflammation predominate in response to H. pylori?
Antrum
232
What do we see here?
H. pylori gastritis
233
What factors does H. pylori secrete?
Urease - neutralizes gastric acid and takes urea to bicarb and ammonia; provides diagnostic test
Virulence factors - proteolytic and glyoclytic enzymes, cytotoxins, breakdwon of acid-protective barriers
234
What is important about H. pylori's urease?
It not only helps the bacteria neutralize gastric acid, but provides a diagnostic test for its presence
235
What can cause multifocal atrophic gastritis (environmental gastritis)?
H. pylori, diet, and other environmental factors
Common in 3rd world countries
10x higher risk for gastric cancer
236
What are etiologies of peptic ulcer disease?
H. Pylori and NSAIDs
237
What proportion of stomach ulcers are caused by H pylori vs NSAIDS/other?
HP = 70%, rest is other
238
What proportion of duodenal ulcers are caused by H pylori vs NSAIDS/other?
HP = 90%, rest is other
239
Where do ulcers arise from MAG?
only in stomach
240
Where do ulcers arise from H. pylori?
20% in antrum
80% in duodenal bulb
241
When do you see gastric metaplasia of the duodenum?
When acid (or excess acid) reaches the duodenum / peptic duodenal ulcers/ with H. pylori
242
How long do peptic ulcers typically take to heal?
~6 weeks - cancer can promote formation of ulcer, so if it takes longer, you may suspect cancer
243
What are some complications of H. pylori?
Chronic gastritis
Gastric peptic ulcer
Duodenal peptic ulcer
Gastric cancer
MALT lymphoma
244
What are risk factors for gastric cancer?
Dietary - smoked, pickled, and grilled foods
Older age
Genetic factors and Fam Hx
Chronic atrophic gastritis (H. pylori, autimmune, environmental)
245
What regions have higher incidences of gastric cancer?
Japan, parts of S. america, parts of china
246
What are the two types of gastric cancer?
Intestinal - relationship to intestinal metaplasia
Diffuse - describes how the cancer spreads
247
Which type of gastric cancer affects males more than females?
"intestinal"
248
Which type of gastric cancer affects females more than males?
"diffuse"
249
Which gastric cancer forms a discrete mass?
"intestinal"
250
Which gastric cancer has ill-defined gross morphology?
"diffuse"
251
Histologically, what do intestinal type gastic cancers look like?
Adenocarcinoma - discrete mass, gland formations
252
How does the intestinal type gastric cancer progress?
253
What is Linitis Plastica?
Rigid, rock-hard thickened stomach
254
What do you see here?
Signet ring cells - indicative of adenocarcinoma, diffuse type gastric cancer
255
What are krukenberg tumors?
Ovarian metastases of gastric cancers
256
What factor gives a favorable prognosis for gastric carcinoma?
Early, submucosal carcinoma vs advanced
257
What are the macroscopic folds of the small intestine called?
Folds of Kerkring (plicae circularis)
258
What is the ratio of the villus:crypt heights?
4-5:1
259
What are the two predominant epithelial cells of the small intestine?
Goblet cells
Columnar cels (enterocytes)
260
Where do epithelial cells of the small intestine originate?
Crypt cells - differentiate and migrate up towards villus
Process takes 5-6 days
261
What are paneth cells?
At the bottom of the crypt
Elaborate enzymes (lysozyme and defensin)
Help protect progenitor cells from damage
262
Where are paneth cells found?
Small intestine
263
What do we see here?
A villus of the small intestine
Note the brush border and the lamina propria
264
How much fluid is presented to the small intestine every day?
8 L
2 from oral intake, the rest is secretions (salivary, gastric, biliary and pancreatic)
265
How much fluid is presented to the colon?
1.5 L (after the small intestine absorbs a lot of fluid and secretes its own)
266
How how much fluid is absorbed by the small intestine?
~12 L
267
What percentage of fluid does the small intestine absorb?
75-80% (colon is \>90%)
268
What is the maximum absorption capacity of the small intestine?
12 L / day (more than that =\> diarrhea)
269
What is the maximum absorption capacity of the colon?
5L (more than that =\> diarrhea)
270
What is the consequence of colonic water reabsorption being a saturable process?
Diarrhea if you can't absorb all you provide
271
What differences do we see between the mucosal epithelium of the small intestine in fasting vs absorptive states?
Fasting = cells packed close together; absorptive = potential space is filled
272
How does water get absorbed in the small intestine?
273
What are differences between the jejuum, ileum and colon with respect to the permeability of the epithelium?
Jejunum allows largest things through, colon smallest
274
What area of the intestines has the highest passive permeability? which has lowest? which has intermediate?
275
How does the net water movement change along the course of the intestine?
276
What are the three ways that sodium is transported?
Apical sodium channel - permits Na entry into cell down electrochemical gradient; Na exits basolateral membrane via Na-K ATPase
Solute-coupled sodium transport - apical membrane, transports Na wiht glucose or aa; basis for oral rehydration therapy of diarrhea
Sodium hydrogen exchanger - permits sodium and chloride entry; HCO3 secretion
277
How does electrogenic sodium absorption work?
Relies on Na-K ATPase on basolateral membrane
278
How does nutrient-coupled sodium transport work?
Can get sodium in if you have glucose to go with it
Also relies on Na-K ATPase basolaterally
279
What is the basis of oral rehydration therapy?
Addition of glucose in the lumen to help bring sodium into the body (water follows)
280
How does sodium-hydrogen exchange and sodium chloride absorption work?
Also important in acid-base balance
281
What factors can stimulate sodium absorption?
Mineralocorticoids - increase absorption more in colon than in small intestine
Glucocorticoids
Somatostatin (ocreotide)
Adrenergic agonists (epi, clonidine)
Also drugs that slow bowel transit (opiates, somatostatin - double whammy)
282
What is the major ion that drives fluid secretion in the small intestine?
Chloride (Cl)
283
How does chloride tranpsort occur?
Cl enters basolaterally (Na:K:2Cl transporter), exceeds electrochemical equilibrium, and exits via apical membrane via Cl channel (CFTR)
284
What factors can increase chloride secretion?
Hormones
Neural input
Inflammatory factors
Infectious factors
Toxins,
etc
All work by activating cAMP, cGMP, and intracellular calcium
285
What transporter gets chloride from the blood stream into the enterocytes?
Na:K:2Cl transporter
286
What channel helps secrete chloride into the lumen of the intestines from the enterocytes?
CFTR (chloride channel)
287
What are some factors that increase/decrease transit time?
288
What does "diarrhea" mean when a patient says it?
Can be:
More frequent stools
Larger volume stools
Looser stools
289
What does diarrhea mean clinically, as a sign?
Stool weight \> 150-200 g/24 hours
Stool water \> 150-200 ml/24 hours
290
What defines acute vs chronic diarrhea?
\<2-3 weeks is acute; \>3 weeks is chronic
Acute is commonly infectious; chronic can be multiple infections
Acute is usually self-limited; chronic is variable
291
What do large-volume diarrhea indicate?
Small intestinal dysfunction
292
What do you see in small intestinal dysfunction wrt stools?
Large large volume
293
What do you see in colonic dysfunction wrt stools?
Large, but not huge volumes
294
What are some characteristics of small bowel and colonic dysfunction?
Large stool volume
Moderate increase in number
Minimal urgency
No tenesmus
Little mucus
295
What are some characteristics of recto-sigmoid dysfunction?
Small amount of stool
Frequency
Urgency
Tenesmus
Mucus
Blood
296
What can differentiate small bowel and colonic from recto-sigmoid dysfunction?
297
What is the effect of bile acid in your colon?
Bile acids induce secretion - ileum is only site of active bile acid absorption
298
What is osmotic diarrhea?
Non-absorbable solute in lumen of bowel
Water enters lumen - at the small bowel with the greatest permeability
Solute and water load exceed colonic absorptive capacity
Mucosal transport processes are typically in tact
299
What are some solutes that can cause osmotic diarrhea?
Lactose
Sorbitol (chewing gum), and other sugar substitutes
Na Sulfate lavage solutions
Magnesium citrate
You do this as prep for colonoscopy
300
Why is osmotic diarrhea not life threatening?
You lose only water, not sodium - so you maintain your intravascular oncotic pressure
301
What happens in osmotic diarrhea when you decrease intake of the agent?
Stool volume decreases
302
What is secretory diarrhea?
Stimulation of normal secretory process
Absorptive processes are intact but overwhelmed
303
What things can cause secretory diarrhea?
Secretagogues that increase cAMP, cGMP, and/or calcium
Bacterial toxins, hormones, bile acids, drugs, inflammatory mediators
304
How does cholera toxin work?
305
What is the effect of fasting on secretory diarrhea?
No effect
306
Is secretory diarrhea life threatening?
YES - salt and water depletion
307
What is motility diarrhea?
Hypermotility - insufficient contact time for absorption (hyperthyroid, cholinergics, laxatives, anxiety)
Hypomotility - stasis and bacterial overgrowth can promote diarrhea
308
What is digestion?
Breaking down food (macronutrients) to smaller, absorbable components
Pre-mucosal (i.e. lumen or brush border membrane)
Absorption is the **transport** of the breakdown products of digestion across the intestinal epithelium; which is "mucosal"
309
What is absorption?
Transporting the breakdown products of digestion across the intestinal epithelium
A "mucosal" process
In contrast to digestion, which is breaking down food and is a pre-mucosal process
310
What is this?
Intestinal epithelium
311
Where is iron absorbed??
Duodenum
312
Where do you absorb you minerals (Ca, Mg, etc)?
duodenum
313
Where do you absorb cobalamin?
Ileum
314
Where do you primarily absorb bile acids?
ileum
315
Where do you absorb carbohydrates?
All along small intestine
316
Where do you absorb protein, lipids, sodium, and water?
All along the small intestine
317
What is the function of secretin?
Hormone - via blood, tells pancreas to tell pancreas to make bicarbonate rich secretion
Slows gastric emptying too
318
What is the result of fatty acids and amino acids reaching the duodenum?
CCK production - gallbladder contracts, and tells pancreas to secrete enzymes
319
How are carbohydrates digested?
Must be hydrolyzed to monosaccharides
320
What is starch?
Polymer of glucose
321
What breaks down starcH/
amylase - converts them into smaller glucose units
322
What does maltase do?
Breaks down disaccharides to monosaccharides (intestine BBM)
323
Where is amylase found?
pancreas, saliva
324
What is sucrose-isomaltase?
Fouond on the intestine BBM and converts sucrose to glucose and fructose (disaccharidase)
325
What is lactase?
Converts lactase to glucose and galactose (foudn in BBM)
326
How is sucrose digested?
Sucrose-isomaltase
327
How is lactose digested?
lactase
328
How are carbohydrates absorbed/
As glucose/galactose
Actively transported into cell, and then diffuse into portal vein
329
What happens to any unabsorbed carbohydrates?
Converted to short chain fatty acids in the colon
Bacteria may also consume it and produce gas
330
What is the schema of carbohydrate digestion?
Then
331
What is the schema of carbohydrate digestion product absorption?
332
How are proteins digested?
Hydrolyzed to oligopeptides or amino acids (4 or 5 aa max)
333
How are proteins digested in the stomach?
HCl denatures protein
Pepsin hydrolyzes protein into polypeptides
334
How are proteins digested in the duodenum and pancreas?
Pancreas releases proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)
Enterokinase in duodenal BBM activates trypsin which then activates other pancreatic pro enzymes
335
How are proteins digested in the small intestine?
BBM oligopeptidases hydrolyze oligopeptides into di- tri- and tetrapeptides and amino acids
336
How are proteins digestion products absorbed?
Amino acids and oligopeptides are absorbed and transported inot capillaries (portal vein)
337
Schema for stomach digestion of proteins
338
What is the role of the pancreas and duodenum in protein digestion?
Pancreatic zymogens are converted inot active enzymes in the duodenum
339
What is the schema of absorption of amino acids and short peptides in the small intestine?
340
How are lipids digested?
Emulsification, lipolysis, micelles
341
What is the role of the stomach in lipid digestion?
Churns fat into an unstable emulsion
342
What is the role of the duodenum and small intestine in lipid digestion?
The emulsion it receives from teh stomach is stabilized by phospholipids from the diet and bile salts from the liver
Dietary fat causes CCK release which activates lipase from the pancreas and bile salt release
Pancreatic lipase and co-lipase convert triglycerides into monoglycerides and free fatty acids
Mixed micelles are created with these on the inside and bile salts on the outside
343
What is the role of pancreatic lipase and co-lipase in lipid digestion?
Converts triglycerides into monoglycerides and free fatty acids
344
How are lipid digestion products absorbed?
Monoglycerides and free fatty acids form micelle wiht bile salts (bile salts on the outside)
Passively diffuse across BBM into cell
Intracellularly, they are resynthesized as chylomicrons and VLDL which are exported into the **lymphatics** (lacteal)
345
Where in the circulation do lipids go once digested?
Long chain triglycerides go to the lymphatics (most)
Medium chain triglycerides go to the portal vein
346
What is teh schema for stomach digestion of lipids?
lipolysis is very little - mostly emulsification
347
What is the schema for fat digestion in the small intestine?
348
What is the schema for lipid product absorption?
349
What is the schema for lipid product absorption and entrance to the circulation?
350
How is vitamin B12 absorbed?
B12 is first bound to haptocorrin (R protein/factor) in saliva
Then swapped out for intrinsic factor (produced by parietal cells) once B12-R is split in the duodenum by trypsin
Then IF-B12 is absorbed in the ileum
Then B12 is transported to portal circulation bound to transcobalamin-II
351
What is the clinical finding you see when you malabsorb protein?
edema
352
What is the clinical finding you see when you malabsorb fat?
steatorrhea, weight loss
353
What is the clinical finding you see when you malabsorb carbohydrates?
diarrhea, bloating, gas
354
What is the clinical finding you see when you malabsorb vit. A?
night blindness, hyperkeratosis
355
What is the clinical finding you see when you malabsorb vit D., calcium?
tetany (muscle spasms/involuntary contractions), osteomalacia
356
What is the clinical finding you see when you malabsorb vitamin E?
Neuropathy
357
What is the clinical finding you see when you malabsorb vit. K?
Ecchymoses
Bruising
358
What is the clinical finding you see when you malabsorb vit B12?
Megaloblastic anemia
Glossitis
Cheilosis
Neuropathy
359
What is the clinical finding you see when you malabsorb Folate?
Megaloblastic anemia
Glossitis
360
What is the clinical finding you see when you malabsorb iron?
Microcytic anemia
Dyspnea
Fatigue
Glossitis
361
Which regions commonly get primary lactase deficiency?
Asians, Africans, Mediterranean descent
362
What can cause secondary lactase deficiency?
Loss of enterocytes (infection, resection, radiation)
363
What are symptoms of lactase deficiency?
Diarrhea, gas, bloating, borborygmi (stomch grumblings)
364
What are ways to diagnose lactase deficiency?
Good history
Hydrogen breath test if needed
365
How does a hydrogen breath test work?
Picks up hydrogen gas produced by bacteria that eat up lactose that you cant digest
Can be used to diagnose lactase deficiency (often not needed)
366
What is the treatment for lactase deficiency?
Avoid dairy
Exogenous lactase
Lactose-free products
367
What is the schema for lactase deficiency?
368
What is the result of pancreatic exocrine insufficiency?
Fat, protein, carbohydrates are all maldigested
369
How much pancreatic function must be lost before you get pancreatic exocrine insufficiency?
90-95% of the pancreatic function
370
What are some examples of things that may cause pancreatic exocrine insufficiency?
Cystic fibrosis (in children)
Chronic pancreatitis
Pancreatic resection
371
How do you diagnose pancreatic exocrine insufficiency?
Usually on x-ray due to calcifications from scarring (or on CT)
372
How do you treat patients with pancreatic exocrine insufficiency?
Oral pancreatic enzyme replacement
Enteric coated (with acid suppressing agent)
373
What do you see in patients with bile salt deficiency?
Difficulty digesting fat/fat-soluble vitamins
374
What are examples of things that can causebile salt deficiencies?
Severe cholestasis
Distal ileal resection or disease (Crohn's) - where it is reabsorbed
Bacterial overgrowth - bacteria make bile salts unusable
375
How do you diagnose bile salt deficiency?
Work-up of underlying disease
376
How do you treat bile salt deficiency?
Treat underlying condition
Feed medium chain triglycerides instead
377
What are factors that protect against bacterial overgrowth?
Gastric acid
Small bowel motility
Ileocecal valve
Secreted immunoglobulins
378
What can cause bacterial overgrowths?
Poor motility
Decreased gastric acid
Connection between colon and small intestine (no ileocecal valve, perhaps, or fistula)
Few immunoglobulins
379
What are some conditions associated with bacterial overgrowth?
Motility disorders (stasis)
Anatomic disorders (fistula, diverticula, blind loop)
380
What are some consequences of bacterial overgrowth?
Fat malabsorption: bacteria conjugate/dehydroxylate bile salts
Vit. B12 deficiency - they consume vit. B12
381
How can you diagnose bacterial overgrowth?
Schilling test, breath test
382
How do you treat bacterial overgrowth?
Correct underlying problem; antibiotics
383
What can cause short bowel syndrome?
Resection (due to chrohn's, infarct, radiation, trauma, cancer)
Bypass (surgical, fistula)
384
What happens if you lose your first 100cm of jejunum?
It is responsible for \>90% of digestion/absorption
385
What happens if you lose your last 100 cm of terminal ileum?
Permanent vit. B12 and bile acid malabsorption
Rapid transit (ileal brake - enteroglucagon, peptide YY)
Cholesterol gallstones (bile salt pool depletion)
Oxalate kidney stones: calcium binds to free fatty acids instead of oxalate; oxalate absorbed in colon
D-lactic acidosis (neuro symptoms, due to colonic bacteria)
386
How do you diagnose a short bowel syndrome?
Small bowel imaging (CT/ MRI)
387
How do you treat short bowel syndrome?
Enteral feeding if possible
Total parenteral nutrition
Small intestine transplant
388
What is celiac disease?
Inappropriate immune response to gliadin (a protein in gluten)
Common in northern European population
389
What occurs histologically in celiac disease?
Villous atrophy
Crypt hyperplasia
Plasma cells in lamina propria
Intraepithelial lymphocytes (IELs)
390
Where along the GI tract does celiac disease affect most?
Proximal more than distal small intestine (thats where the gliadin first hits)
391
What are immunological abnormalities seen in celiac disease?
HLA-DQ2, DQ8
selective IgA deficiency, diabetes, autoantibodies
392
What are some associations/complications with celiac disease?
Dermatitis herpetiformis (skin rash)
Collagenous sprue
T cell lymphoma
393
How do you diagnose celiac disease?
Small bowel biopsy pre and post diet
Autoantibodies
394
How do you treat celiac disease?
Eat a gluten-free diet
395
What do you see here?
Active Celiac sprue
Villous atrophy
Crypt hyperpasia
Inflammation of lamina propria
396
What is tropical sprue?
Acquired syndrome - some bug yet unidentified
Affects entire small bowel (proximal and distal)
Similar to celiac
397
What is the difference in location of disease in tropical sprue and celiac sprue?
Tropical is all throughout small bowel
Celiac is more proximal
398
What are differences between tropical and celiac sprue?
399
What is abetalipoproteinemia?
Autosomal recessive disease
Epithelial cells cannot assemble chylomicrons, so lipid accumulates in cells
Fat malabsorption
Diagnose with small bowel biopsy
Treat with dietary fat restriction
400
What is this?
Abetalipoproteinemia
401
How do you diagnose abetalipoproteinemia?
Small bowel biopsy
402
How do you treat abetalipoproteinemia?
Dietary fat restriction
Medium chain triglyceride oil
403
How do you test for malabsorption?
Blood tests and specialized tests
404
What can a CBC show malabsorption for?
Anemia - micro or macrocytic
405
What does microcytic anemia indicate?
Iron deficiency (malabsorption)
406
What does macrocytic anemia indicate?
B12 or Folate deficiency
407
What does low albumin indicate?
Protein malabsorption
408
What does low calcium indicate?
Vit. D or calcium malabsoroption (duodenal disease)
409
What does prolonged prothrombin time indicate?
Vitamin K deficiency or malabsorption -\> fat absopriton issue (vit. A, D, E, K)
410
What is a fecal fat analysis useful for?
Quantify steatorrhea - to identify pancreatic disease
411
What does a D-xylose test help identify?
Small bowel disease
412
How does a D-xylose test work?
xylose is monosaccharide - should enter body easily
~25% of injested xylose should be measured in urine. If lower: problem w/ small bowel, or less likely, liver disease or bacterial overgrowth
413
How do you workup fat malabsorption?
72 hour fecal fat followed by D-xylose test if abnormal
414
What is Meckel's Diverticulum?
Most common congenital anomaly of the GI tract
Outpouching of the small intestine from failure of vitelline duct closing
415
What is this?
Meckel's Diverticulum
416
Where is Meckel's Diverticulum located?
2 feet from the colon and close to the appendix grossly
417
What are the two most common heterotopic tissues seen with Meckel's Diverticulum?
gastric -\> peptic ulcer
pancreatic -\> not many symptoms
418
How do you perform a Meckel's Scan?
Tectecium - seen in stomach - also can be seen in Meckel's Diverticulum if you have heterotopic tissue excreting acid
419
What are problems with extrinsic obstructions of the small intestine?
Intestinal ischemia - requires multiple blood vessels to be obstructed or flow from SMA
420
Why is the small intestine susceptible to esxtrinsic mechanical obstruction?
Pliant wall
Narrow lumen
Long length
421
Why is it difficult to get intestinal ischemia of the small intestine (and why is it a problem if you do get it)?
Many collateral circulations
Ischemia means that either SMA flow is compromised or multiple blood vessels are compromised
422
What are sources of extrinsic obstruction of the bowel that can cut off multiple blood vessels?
Strangulated hernia
Volvulus
Intussusception
423
What do extrinsic obstructions of the small intestine have in common?
Distended
Reddish necrotic color
Exudate often seen
e.g.
424
What is a hernia?
Weakness in peritoneum- intestines pouch out
Typically reducible (can be pushed back)
Can compress veins and arteries (can cause extrinsic obstruction)
425
What is volvulus?
Bowel twisted upon itself
426
What are risk factors for volvulus?
Adhesions (after surgery, or congenitally, for example)
Poor motility (diabetics, neurologic diseases)
Abnormal mesentery
Congenital malrotation
427
What is intussusception?
One part of bowel is swallowed up by another part
Leading point is a mass lesion - in adults usually benign or malignant lesion treated by surgery
In children it is usually hyperplastic lymphoid tissue that requires retrograde barium enema to reverse the intussusception
428
What is the common cause of intussusception in adults?
Benign or malignant tumor - surgery removes it
429
What is the common cause of intussusception in children?
Hyperplastic lymphoid tissue - treat with retrograde barium enema to reverse intussusception
430
What causes intussusception?
Mass lesion as leading point (children = lymphoid tissue; adults = tumors)
431
What is gluten sensitive enteropathy?
Celiac disease
432
What is the protein that is the source of celiac disease?
Gliadin - in gluten
433
What is an inflammatory disease triggered and maintained by exposure to gliadin?
Celiac disease
434
Approximately how many north americans have celiac disease?
0.111111111
435
How many celiac disease patients are symptomatic?
20%
436
What are the two implicated HLA types in celiac disease?
95% HLA-DQ2
5% HLA-DQ8
437
What is an important serum marker for Celiac Disease?
Circulating IgA antitissue transglutaminase (TGT)
Indicator of active disease too
438
When does Celicac Disease typically onset?
At any age
At infancy you are exposed to cereals
439
What are symptoms of celiac disease?
Steatorrhea
Failure to thrive
Short stature
Calcium malabsorption, osteoporosis - proximal small bowel absorbs nutrients
Iron-deficiency anemia - proximal small bowel absorbs nutrients
Infertility
440
Disease progression from normal on left to severe on right. What disease is this?
Celiac Disease
Partial then total villous atrophy
441
What can be found in the surface epithelium in Celiac Disease?
Intraepithelial lymphocytes
442
What do we see here? 
Intraepithelial lymphocytes characteristic of Celiac Disease
443
What finding do you see in the crypts in Celiac Disease?
Increased crypt mitoses
444
What finding do you see here?
Increased crypt mitoses - Celiac Disease
445
What histological finding do you see in the lamina propria in Celiac Disease?
Chronic inflammation
446
What is this finding?
Chronic inflammation in Celiac Disease
447
What factor correlates with the severity of malabsorption in Celiac Disease?
Severity of villous atrophy
448
What factors go into the diarrhea seen in Celiac Disease?
Attenuated glycocalyx -\> impaired digestion; lactase deficiency
Attenuated microvilli -\> attenuated absorption
Damaged organelles -\> impaired metabolism and absorption
449
What are some diseases associated with Celiac Disease?
Ulcerative jejunoileitis
Enteropathy-associated T cell lymphoma
GI & non-GI cancers
Dermatitis Herpetiformis
Collagenous sprue
450
What is Whipple's Disease?
Rare multisymptom disease (GI, eyes, skin, joints, heart, liver, brain, etc)
Caused by *Trophyrema whipplei* - intracellular bacilli (similar to M avium)
Numerous "foamy" PAS+ macrophages
Diagnosed with PCR
Treated w/ Abx
451
What organism causes Whipple's DIsease?
Trophyrema whipplei
452
What is Trophyrema whipplei?
Intracellular bacillus related to M. avium that causes Whipple's Disease
453
What is the treatment for Whipple's Disease?
Antibiotics - caused by Trophyrema whipplei
454
What is the diagnostic test for Whipple's Disease?
PCR for Trophyrema whipplei
455
What causes obstruction in the case of Whipple's Disease?
Lymphatic obstruction due to bacterial infection
456
What is Congenital Lymphangiectasia?
Rare genetic disease caused by germline mutation of VEGFR-3 that presents with generalized malformations of lymphatic system
Asymmetrical edema, chylous ascites
Engorged lacteals - loss of protein and lymphocytes into gut
Malnutrition, lymphocytopenia, recurrent infections
457
What are some symptoms of congenital lymphangiectasia?
Asymmetrical edema
Chylous ascites
Malnutrition, lymphocytopenia, recurrent infections
458
What gene causes Congenital lymphangiectasia?
VEGFR-3
459
What is a danger of small intestinal diverticuli?
Bacterial overgrowth
460
What is this?
Small intestinal diverticulosis
Can cause bacterial overgrowth and lead to malnutrition
461
What is a true diverticulum?
All layers of intestinal wall present
462
What is a false diverticulum?
Mucosa only
463
What is the only true diverticuluM?
Congenital - e.g. Meckel's
464
What history items are crucial for a nutritional assessment?
Weight loss
Food intake
Malabsorption
Micronutrient deficiencies
465
What physical exam markers are important for a nutritional assesment?
Weight/BMI
Anthropometrics
Tissue depletion
Hydration status
466
What are important laboratory markers of nutritional assessment?
Albumin
Transferrin
Transthyretin
467
What does mild/moderate malnutrition look like?
BMI 16-18.5
Weight loss of 5-10%
Functional Impairment
468
What does severe malnutrition look like?
BMI \< 16
Weight loss \> 10%
Muscle Wasting
Functional Impairment
469
What are the three ways we expend energy?
Resting energy expenditure (REE) - 70%
Energy expenditure of physical activity - 20%
Thermic effect of feeding - 10%
470
What is a normal intake for a healthy adult?
20-25 kcal/kg
471
What are the three sources of energy in a western diet?
Protein 10-15% (4cal/g)
Carbohydrates 55% (4cal/g)
Fats 30% (9cal/g)
472
What is the most energy rich food?
Fats (9cal/g)
473
What are micronutrients?
Don't give energy, but crucial
Vitamins (Fat and water soluble) and minerals
474
What are macronutrients?
Give energy
Protein, carbohydrates, fats
475
What is primary protein energy malnutrition?
Inadequate nutrient intake (may be due to a variety of things)
476
What is secondary protein energy malnutrition?
Elevated requirements in the face of illness/injury with relative inadequate intake (not necessarily an intake problem)
477
What is kwashiokor?
Protein malnutrition
Presents with edema, lethargy, low serum albumin
478
What is protein malnutrition with edema, lethargy, and low serum albumin known as?
Kwashiokor
479
What is marasmus??
Total malnutrition
With weight loss, muscle mass and subcutaneous fat loss and normal serum albumin
480
What malnutrition is of all macronutrients, presents with weight loss, muscle and subcutaneous fat loss and with normal serum albumin?
Marasmus
481
When do you provide nutrition support?
Acutely Ill
Moderate-Severe malnutrition
Unable to meet nutritional needs within 48 hours
Malnourished and need major surgery
482
What BMI defines "underweight"
\<18.5
483
What BMI range is normal?
18.5 - 24.9
484
What BMI defines "overweight"?
25-29.5
485
What defines Class I obesity?
30-34.9
486
WHat defines Class II Obesity?
35-39.5
487
What defines Class III obesity?
\>40
488
How do you assess obesity in pediatric patients?
By BMI percentile
489
What are some genetic causes of obesity?
Prader-Willi, Bardet Biedl, Leptin deficiency
Very rare
490
What are medical conditions that can lead to obestiy?
Cushings Syndrome
Hypothyroid
Hypothalamic Injury
Rare
491
What are environmental factors that can cause obesity?
Smoking cessation
Post pregnancy
Sleep deficiency
492
What are the brakes in feeding?
POMC and CART make α-MSH to stop hunger
493
Where is leptin produced?
Adipose tissue
494
What ist he target of leptin?
Hypothalamus
495
What is the action of leptin?
Decrease energy intake
