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GI and Liver > GI Deck 1 > Flashcards

GI Deck 1 Flashcards

1
Q

What is the distance between the incisors to the stomach?

A

40 cm

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2
Q

What is the position of the esophagus in the thoracic cavity?

A

posterior

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3
Q

What muscles make up the upper esophageal sphincter?

A

Lower fibers of inferior pharyngeal constrictor

Cricopharyngeus

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4
Q

What is the state of the upper esophageal sphincter at rest?

A

Tonically closed

Relaxes during a swallow

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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

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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

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7
Q

Is the LES a true sphincter?

A

No - it is a high pressure zone

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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.

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9
Q

What neural factors increase LES pressure?

A

Cholinergics

α- adrenergic agonists

β-adrenergic blockers

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10
Q

What hormones can increase LES pressure?

A

Gastrin

Motilin

Substance P

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11
Q

What food can increase LES pressure?

A

Protein

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12
Q

What drugs can increase LES pressure?

A

Pro-kinetics (metoclopramide, doperidone)

Histamine

Antacids

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13
Q

What neural factors decrease LES pressure?

A

Cholinergic antagonists

α adrenergic blockers

β- adrenergic agonists

Nitric oxide

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14
Q

What hormones can decrease LES pressure?

A

Secretin

CCK

Somatostatin

Progesterone (e.g. pregnancy)

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15
Q

What foods can decrease LES pressure?

A

Fats

Chocolate

Ethanol

Peppermint

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16
Q

What drugs can decrease LES pressure?

A

Theophylline

Ca- channel blockers

Morphine

Diazepam

Serotonin

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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)

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18
Q

What is dysphagia??

A

Sense of impaired transport of bolus through esophagus

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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

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20
Q

What is odynophagia?

A

Pain on swallowing

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21
Q

What does the chest pain of esophageal disorder typically mimic?

A

Angina pectoris

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22
Q

What is regurgitation with respect to esophageal disorder?

A

Entry of gastric contents inot esophagus or mouth

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23
Q

What does a barium esophagram tell you?

A

Evaluates a structural lesion (stricture, web, hiatal hernia)

Can sometimes demonstrate GE reflux

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24
Q

What does an endoscopy with biopsy of the esophagus tell you?

A

Directly visualizes esophageal mucosa

Enables tissue diagnosis

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25
Q

What does endoscopic ultrasound (esophageal) tell you?

A

Useful for imaging lesions that are in esophageal wall or immediately adjacent to esophagus

Fine needle aspirate is possible

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26
Q

What do we see here?

A

Esophageal cancer

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27
Q

What is esophageal monometry useful for?

A

Measures pressures, contractile activity and sphincter function

Useful for motility disorders

Can demonstrate tendency for GE reflux

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28
Q

What do acid reflux (pH) studies tell you?

A

Measures esophageal pH

24-hour pH probe

Quantitates teh amount and duration of reflux

Can correlate with symptoms

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29
Q

What is GERD?

A

Gasroesophageal refulx disease

Casued by reflux of gastric contents into the esophagus

Not all reflux causes disease (not all reflux is acid)

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30
Q

What causes GERD?

A

Reflux of gastric contents into esophagus

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31
Q

What are symptoms of GERD?

A

Heartburn (worse with food, lying supine, better with antacids)

Chest pain, dysphagia, hoarseness

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32
Q

What are key diagnostic tests for identifying GERD?

A

History

24-hour pH monitoring (reflux itself)

Endoscopy for the effects of reflux

LES pressure and barium swallow for the potential to reflux

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33
Q

What are the aggressive pathogenic factors of GERD?

A

Acid (or bile)

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34
Q

What are defensive pathogenic factors of GERD?

A

Anti-reflux barrier (LES and crural diaphragm)

Esophageal acid clearance (saliva, esophageal peristalsis, gastric emptying, intact esophageal mucosa, hiatal hernia)

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35
Q

What is the most important defensive factor against the development of GERD?

A

Anti-reflux barrier

LES and Crural diaphragm

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36
Q

What are issues with esophageal acid clearance that can lead to GERD?

A

Reduced saliva production

Malfunctioning esophageal peristalsis

Faulty gastric emptying

Non-intact esophageal mucosa

Hiatal hernia –> more acid in the esophagus –> GERD (thanks SFong!)

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37
Q

What do we see here?

A

GERD

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38
Q

What is a hiatal hernia?

A

Increase in transient LES relaxations (TLESRs)

Acid pocket within proximal stomach

Loss of crural pinch at the GE junction

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39
Q

What are the two types of hiatal hernias?

A

Sliding and para-esophageal

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40
Q

What is this?

A

Sliding hiatal hernia

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41
Q

What is this?

A

Para-esophageal hiatal hernia

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42
Q

What test do you perform to demonstrate increased acid exposure?

A

24-hr pH

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43
Q

What test do you do to correlate acid exposure to symptoms in GERD?

A

24-hr pH

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44
Q

What test do you perfrom to show evidence of mucosal disease in GERD?

A

Endoscopy

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45
Q

What test do you perform to identify the mechanisms of reflux in GERD?

A

Esophagram or manometry

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46
Q

What are complications of GERD?

A

Mucosal ingury (esophagitis, ulcer)

Stricture

Barret’s metaplasia (squamous epithelium changes to columnar epithelium - premalignant)

Esophageal adenocarcinoma

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47
Q

What algorithm do you follow to identify the cause of dysphagia?

A
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48
Q

What is the first question you ask a patient with dysphagia??

A

Solids or liquids?

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49
Q

What test can you use to identify a mechanical vs a motor disorder of dysphagia?

A

Structural first (endoscopy or barium swallow)

Followed by esophageal manometry

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50
Q

What is achalasia?

A

Failure of smooth muscle fibers to relax, which can cause a sphincter to remain closed and fail to open when needed (LES)

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51
Q

What ist he pathogenesis of achalasia?

A

Loss of inhibitory ganglion cells within myenteric plexus

LES remains tonically contracted

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52
Q

What are abnormalities seen on manometry in achalasia?

A

Hypertensive LES

Impaired LES relaxation

Aperistalsis of body of esophagus

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53
Q

What are clinical symptoms of achalasia?

A

Dysphagia

Regurgitation

Eventual weight loss

Chest pain

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54
Q

What od we see here?

A

Achalasia

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55
Q

What do we see on the right?

A

Achalasia

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56
Q

How do you treat achalasia?

A

Botulinum toxin

Pneumonic dilation

Heller myotomy

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57
Q

What diseases cause pseudo-achalasia?

A

Chagas’ disease (trypanosma cruzii infection)

Cancer of GE junction (more rapid onset, more weight loss)

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58
Q

What do you see on barium swallow in scleroderma?

A

Loss of LES function (GE reflux)

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59
Q

What do you see in manometry in scleroderma?

A

Poor esophageal motility

Low LES pressure

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60
Q

What is diffuse esophageal spasm?

A

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.

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61
Q

What are symptoms of diffuse esophageal spasm?

A

Chest pain, odynophagia or both

May mimic angina pectoris

On X-ray you can see corkscrew esophagus

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62
Q

What is this?

A

Diffuse esophageal spasm (corkscrew esophagus)

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63
Q

What do you see on manometry in diffuse esophageal spasm?

A

Simultaneous contractions

Repetitive contractions

LES usually normal

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64
Q

What do we see on the right?

A

Diffuse esophageal spasm

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65
Q

How do you treat diffuse esophageal spasm?

A

Muscle relaxants

Calcium-channel blockers

Nitrates

Rarely surgery

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66
Q

What is nutcracker esophagus?

A

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

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67
Q

What esophageal disease on manometry has normal amplitude contractions with abnromal contraction frequencies?

A

Diffuse esophageal spasm

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68
Q

What esophageal disease has abnormal amplitude contractions (high) with normal peristalsis and LES?

A

Nutcracker esophagus

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69
Q

What are features of manometry of nutcracker esophagus?

A

High amplitude contractions

Normal peristalsis and LES

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70
Q

What do we see on the right?

A

Nutcracker esophagus

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71
Q

What part of the GI is this?

A

Esophagus

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72
Q

Identify the mucosa

A
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73
Q

Identify the salivary duct

A
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74
Q

Identify the muscularis mucosae, submucosa

A
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75
Q

Identify a mucous salivary gland

A
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76
Q

Identify the muscularis propria

A
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77
Q

Identify the smooth muscle

A
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78
Q

Identify the myenteric plexus

A
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79
Q

Identify the skeletal muscle

A
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80
Q

Which part of the esophagus do you have skeletal muscle?

A

Proximal (upper 1/3)

Distal esophagus only has smooth muscle

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81
Q

Where do new squamous cells in the esophagus come from?

A

Stem cells - basal cells - mature cells

These then flatten and desquamate at sufrace

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82
Q

What is the “Z” line?

A

Line between stomach and esophagus

esophagus = lighter/shinier

stomach = pinker

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83
Q

What can cause chemical esophagitis?

A

Injury and complications due to household and gardening chemicals, etc

Nature of injury depends on chemical

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84
Q

What is significant about alkalies with respect to chemical esophagitis?

A

Can be odorless and tasteless and can cause rapid injury

They are especially dangerous

Can cause necrosis, saponification, perforation and death

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85
Q

What are some long-term complications of chemical esophagitis?

A

Chronic ulcer, scarring, stricture and eventually squamous cell carcinoma

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86
Q

Why can pills cause damage to esophagus?

A

Pill sticks to mucosa - causes prolonged contact with mucosa

Perhaps during sleep - pill becomes sandwiched in collapsed esophagus

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87
Q

What do you see on endoscopy that is characteristic of esophagitis due to pills?

A

“Kissing ulcers”

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88
Q

Why do pills commonly cause damage to an esophagus during sleep?

A

Pill becomes sandwiched in collapsed esophagus, there are no secretions swallowign or peristalsis, so it can cause injury

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89
Q

What does esophagitis due to pills feel like/present like?

A

Acute chest pain

It is self-limited though

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90
Q

What is particular about the esophagitis that is caused by bisphosphanates?

A

Reacts to produce corrosive compound in stomach.. If any regurgitation/reflux, it will damage the distal esophagus

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91
Q

What is the most common infectious esophagitis?

A

Candida esophagitis

Immunocompromised (but not always)

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92
Q

What are signs and symptoms of candida esophatitis?

A

Odynophagia (painful swallowing)

Oral thrush

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93
Q

What do you find on endoscopy of candida esophagitis?

A

Whitish plaques, desquamated cells and fungi

Stains

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94
Q

Which patients get CMV esophagitis?

A

Exclusively immunocompromised patients

Indicative of viremia (you don’t get local infection)

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95
Q

Which cells of the esophagus does CMV infect?

A

Mesenchymal cells (endothelium, fibroblasts, myocytes)

Does NOT infect squamous cells

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96
Q

What is this?

A

Cytomegalic endothelial cells due to cytomegalovirus (CMV)

CMV esophagitis

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97
Q

Who does herpers esophagitis affect?

A

Immunocompetent or immunocompromised hosts

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98
Q

What cells does herpes esophagitis affect?

A

Squamous cells

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99
Q

What occurs pathologically in herpes esophagitis?

A

Cell-cell detachment

Multinucleation

“Ground glass” nuclei

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100
Q

What do we see here?

A

Herpes esophagitis

Cell-cell detachment

Multinucleation

“Ground glass” nuclei

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101
Q

What area of the esophagus do you want to take a biopsy if you suspect CMV or herpes esophagitis?

A

The border between ulcerated and intact esophagus epithelium

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102
Q

What are some risk factors for reflux esophagitis?

A

LES inocmpetence

High abdominal pressure

Reduced saliva

Other (bulimia, NG intubation)

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103
Q

What causes reflux esophagitis?

A

Injury due to gastric acid, pepsin and duodenal contents (trypsin, bile)

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104
Q

What area of the esophagus is most affected by reflux esophagitis?

A

Distal

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105
Q

What do we see here?

A

GERD

Congested capillaries

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106
Q

What do you see in reflux esophagitis on histology?

A

Edema (wide intracellular spaces)

Ballooned squamous cells

Basal cells hyperplasia

Eosinophils

Congested capillaries

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107
Q

What do you see here?

A

Reflux esophagitis

Edema

Balloooned squamous cells

Basal cell hyperplasia

Eosinophils

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108
Q

What do you see here?

A

Ulcer exudate

Reflux-associated (peptic) ulcer

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109
Q

What are complications of esophageal ulcers?

A

Scarring and stricture (dysphagia)

Regeneration and development of Barrett esophagus

During ulcer - odynophagia, hematemesis (vomit blood)

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110
Q

What is eosinophilic esophagitis?

A

2nd most common esophagitis (and rising)

Dysphagia and food impaction

Antigen driven - 75% have allergic overlay

Treated with dietary restriction, steroids

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111
Q

What type of esophagitis has an allergic component?

A

Eosinophilic esophagitis

(treated as such - restriction of antigen (diet) or steroids)

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112
Q

What is this?

A

Eosinophilic esophagitis

Transverse rings (trachealization)

Longitudinal furrows

Tiny white mucosal plaques

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113
Q

What is this?

A

Eosinophilic esophagitis

Note the eosinophil aggregates near surface and the fibrosis at base

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114
Q

How do you distinguish eosinophilic esophagitis from GERD with respect to age of patient?

A

EoE - children and adults

GERD = adults usually

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115
Q

How do you distinguish eosinophilic esophagitis from GERD with respect to symptoms

A

EoE = dysphagia, food impaction

GERD = heartburn

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116
Q

How do you distinguish eosinophilic esophagitis from GERD with respect to etiology

A

EoE = food and airborne allergens

GERD = gastroduodenal reflux

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117
Q

How do you distinguish eosinophilic esophagitis from GERD with respect to pathogenesis?

A

EoE = IgE and cell mediated injury

GERD = chemical

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118
Q

How do you distinguish eosinophilic esophagitis from GERD with respect to site of injury?

A

EoE = pan-esophageal

GERD = distal

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119
Q

How do you distinguish eosinophilic esophagitis from GERD with respect to therapy?

A

EoE = food restriciton, steroids

GERD = suppression of acid secretion and reflux

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120
Q

What is Barrett esophagus?

A

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

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121
Q

What are characteristics of Barrett esophagus?

A

Salmon-colored mucosa

Circumferential, tongues, islands (<3cm = short-segment Barrett Esophagus)

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122
Q

What is this?

A

Barrett esophagus

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123
Q

If this was taken from an esophagus, what do you suspect?

A

Barrett esophagus - metaplasia

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124
Q

What are the steps between Barrett esophagus to adenocarcinoma?

A

Barrett esophagus -> low grade -> high grade -> cancer

This takes years but patients usually don’t know

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125
Q

How do you diagnose Barett esophagus?

A

Endoscopy and biopsies for dysplasia

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126
Q

Can you visualize dysplasia of Barett Esophagus endoscopically?

A

NO - need biopsy

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127
Q

How do you manage Barrett esophagus?

A

Aggressive treatment of GER

Endoscopic surveillance

Ablation or surgery

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128
Q

What is the progression seen here in the esophagus?

A

Barrett esophagus to adenocarcinoma

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129
Q

Who is the main group of patients who get Barrett adenocarcinoma?

A

White males

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130
Q

What are risk factors for Barrett adenocarcinoma?

A

Duration, and lenght of Barrett esophagus

Dysplasia and genetic factors

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131
Q

What are symptoms of Barrett adenocarcinoma?

A

Dysphagia (solids then liquids)

Weight loss

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132
Q

What is squamous cell carcinoma?

A

Carcinoma arising directly from the squamous cells of the esophagus

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133
Q

What are risk factors for squamous cell carcinoma?

A

Underdeveloped regions - dietary deficiencies, aflatoxins, indoor coal burning

Industrialized countries - alcohol and smoking (synergistic)

Other - achalasia, lye stricture, celiac disease

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134
Q

In the US what demographics get squamous cell carcinoma more commonly?

A

Males more than females

Age > 50

Smoking + alcohol history

Urban > rural environments

Higher incidence in African americans

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135
Q

What does it mean if a patient with squamous cell carcinoma present with symptoms?

A

Advanced disease more commonly

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136
Q

What are clinical features of squamous cell carcinoma?

A

Progressive dysphagia

Weight loss

Hemoptysis, hematemesis

Hoarseness (tumor invasion of recurrent laryngeal nerve)

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137
Q

What do you see here?

A

Squamous cell carcionma - white = squamous cells

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138
Q

What is the natural history of squamous cell carcinoma?

A

Median survival is less than 1 year

5 year survival is 5-10%

Most deaths occur from complications, not metastases

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139
Q

What is the cause of mortality in squamous cell carcionmas?

A

Mostly local complications, not metastases

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140
Q

What do you see here?

A

Squamous cell dysplasia, a precursor of squamosu cell carcinoma

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141
Q

What is squamous cell dysplasia?

A

Precursor to squamous cell carcinoma

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142
Q

Where is the cardia of the stomach?

A

Where esophagus joins the stomach

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143
Q

How many layer of muscles does the stomach have?

A

3

Oblique layer, circular layer, longitudinal layer

These are seperate from muscularis mucosae of the mucosa

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144
Q

What are the layers of the stomach?

A

Mucosa

Submucosa

Muscularis externa

Serosa

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145
Q

Where do you find fundic glands?

A

Proximal stomach

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146
Q

Where do you find pyloric glands?

A

Distal stomach

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147
Q

What do parietal cells produce?

A

Acid (HCl)

Intrinsic factor

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148
Q

What do chief cells produce?

A

Pepsinogen

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149
Q

How do parietal and chief cells work together to promote digestion?

A

Parietal cells produce the acid that helps cleave pepsinogen (produced by chief cells) to pepsin

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150
Q

Where are the stem cells in the stomach mucosa found?

A

Neck cells in a gastric pit

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151
Q

What do ECL cells produce?

A

Histamine

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152
Q

What do the foveolar cells produce?

A

Mucous

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153
Q

What are the red cells?

A

Foveolar

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154
Q

What are the yellow cells?

A

Mucous neck cells

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155
Q

What are the green cells?

A

Parietal cells

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156
Q

What are the purple cells?

A

Chief cells

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157
Q

Identify the layers/cells

A
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158
Q

What is difference between pyloric glands and fundic glands?

A

Pyloric has G cells (make gastrin)

In the gland part- you see mucous producing cells too

Pyloric in antrum

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159
Q

What do G cells make?

A

Gastrin

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160
Q

What are the functions of the stomach?

A

Mechanical churning of food

Initiates chemical digestion of food

Produces intrinsic factor (for vit B12)

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161
Q

How does the stomach initiate the chemical digestion of food?

A

Acid degrades protein

Pepsin begins protein digestion

Lipase digests fat (minor function)

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162
Q

What is the funciton of the fundus and body (proximal portion) of the stomach?

A

Storage and secretion

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163
Q

What is the function of the antrum (distal stomach)?

A

Mixing and grinding

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164
Q

What factors decrease the rate of gastric emptying?

A

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

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165
Q

What is the effect of acid in the duodenum?

A

Triggers secretin production which will feed back and decrease gastric emptying

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166
Q

What is the result of amino acids and fatty acids in the duodenum?

A

trigger cholecystokinin production (CCK) which feeds back and decreases gastric emptying

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167
Q

What is the “ileal brake”?

A

Carbohydrates in the ileum will trigger peptide YY which will result in decreased gastric emptying

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168
Q

What effect do carbohydrates in the ileum produce?

A

Peptide YY production which feeds back to decrease gastric emptying

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169
Q

What is motilin?

A

Pro-kinetic hormone made in the duodenum

Binds to receptors on smooth muscle throughout gut

Increases phase III contractions of migrating motor complex

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170
Q

What drug is a motilin agonist?

A

Erythromycin - produces stomach cramps

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171
Q

What GI side effect is common with erythromycin?

A

Motilin agonist which causes cramps

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172
Q

What is one of the most potent stimuli for gastric secretion?

A

Gastric distention

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173
Q

What is the result of gastric distention?

A

Increased secretions (acid, pepsin, gastrin)

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174
Q

What is GRP?

A

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)

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175
Q

What stimulates parietal cells to produce acid/intrinsic factor?

A

Vagal activity

Gastric distention

Gastrin

Histamine

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176
Q

What stimulates chief cells to produce pepsinogen I and II?

A

Vagal activity

Gastric distention

Gastrin

Histamine

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177
Q

Why do parietal cells have evaginations on their apical surface?

A

To increase surface area to allow for more proton pumps to be able to locate and secrete acid

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178
Q

What are the three receptors on a parietal cells?

A

CCK-B = binds gastrin

H2 = binds histmaine

M3 = binds ACh

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179
Q

How do parietal cells secrete acid in result from a stimulus (say from gastrin or histamine)?

A

Receptor binding causes resting pumps to locate to apical surface and pump out acid

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180
Q

Where do G cells live?

A

antrum of stomach

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181
Q

What is the effect of gastrin?

A

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

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182
Q

What is the role of ECL cells in digestion?

A

Secrete histamine in response to gastrin (from G cells)

Histamine acts on parietal cells to stimulate acid production

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183
Q

What is the role of acetylcholine in parietal cell acid control?

A

Acts directly and indirection (via ECL cells) to increase acid secretion

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184
Q

What hormone is secreted by D cells?

A

somatostatin - turns of G cell gastrin

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185
Q

What is the effect of somatostatin on G cells?

A

Turns off gastrin production

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186
Q

What is the “pH meter” of the GI?

A

D cells - too acidic = turns off signals to produce acid

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187
Q

Why doesn’t the stomach digest itself?

A

There is the mucus-bicarbonate layer

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188
Q

What is significant of the mucus-bicarbonate layer with respect to disease?

A

It provides a relatively neutral niche wherein H. pylori can camp out

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189
Q

What is the effect of NSAIDs on the mucous-bicarbonate layer?

A

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

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190
Q

What is gastritis?

A

superficial erosions of the stomach wall - don’t go very deep

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191
Q

What are gastric ulcers/how are they different from gastritis?

A

They go deep - have a whitish exudate over them

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192
Q

What is this?

A

Gastric ulcer

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193
Q

What is generally the cause of duodenal ulcers?

A

Hypersecretion of acid

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194
Q

What is generally the cause of gastric ulcers?

A

Disruption of mucous barrier (NSAIDs, aspirin)

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195
Q

What infection can cause duodenal ulcers?

A

H. pylori

Suppresses D cells which results in acid hypersecretion (via unopposed gastrin)

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196
Q

What are hte major causes of peptic ulcer disease?

A

H. pylori

NSAIDs, aspirin

Stress (due to ischemia) = major burns, or head trauma

Gastrinoma

(rare = systemic mastocytosis causes histamine; basophilic leukemia produces histamine)

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197
Q

What is the route of transmission of H. pylori?

A

Probably fecal-oral early in life

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198
Q

What is the only known reservoir of H. pylori infection?

A

gastric mucosa

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199
Q

What types of epithelium does H. pylori infect?

A

Gastric type only

Not intestinal or squamous

200
Q

What is a major effect on the normal mediators of digestion that H. pylori affects?

A

Inhibits somatostatin by antral D cells = permits increase in gastrin production which promotes acid hypersecretion

201
Q

What is Zollinger-Ellison Syndrome?

A

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
Q

How do peptic ulcers present?

A

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
Q

How are peptic ulcers treated?

A

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
Q

What are surgical treatment strategies for peptic ulcer disease?

A

Vagotomy - but blocks motility

Cut and re-attach (Billroth) antrectomy

205
Q

What is a roux-en-Y anastomosis?

A
206
Q

What can cause hypergastrinemia?

A

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
Q

What is dangerous about acute erosive gastritis?

A

Potential for serious bleeding

208
Q

What is the etiology of acute erosive gastritis?

A

Drugs, especially NSAIDs

Severe physiologic stress (stress ulcers)

209
Q

What are Curling ulcers?

A

Following burns

210
Q

What are Cushing ulcers?

A

Following brain trauma or surgery

211
Q

What do we see here?

A

acute erosive gastritis

212
Q

What is “chemical” gastropathy?

A

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
Q

What do you see here in these gastric pits?

A

Gastropathy - loss of epithelial mucin; dilated capillaries; “corkscrew” gastric pits

214
Q

When do you see “corkscrew” gastric pits?

A

Gastropathy (no inflammation)

215
Q

When you see erythema on endoscopy of the stomach, what are you considering?

A

Gastropathy (will not see inflammation on biopsy)

216
Q

What do you see in these gastric pits?

A

Chronic gastritis - mucosa infiltarated by mononuclear inflammatory cells and eosinophils

217
Q

What do you see microscopically in chronic gastritis?

A
218
Q

What is a problematic progression of chronic gastritis?

A

Atrophic gastritis - atrophy (loss of glands) and/or intestinal metaplasia

219
Q

What do oyu see here?

A

Atrophic gastritis with intestinal metaplasia

A sequellae of chronic gastritis

220
Q

What part of the stomach does autoimmune gastritis afflict?

A

Body of the stomach

221
Q

What part of the stomach does H. pylori gastritis afflict?

A

Antrum

222
Q

What part of the stomach does multifocal atrophic gastritis afflict (MAG)?

A

Pangastritis (all)

223
Q

What are key features of chronic autoimmune gastritis?

A

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
Q

Normal is on the left, what do you see on the right?

A

Chronic autoimmune gastritis

Reduced glands, loss of parietal and chief cells

Replacement by antral and intestinal epithelium (metaplasia)

Chronic inflammation

225
Q

What are gross features of chronic autoimmune gastritis?

A

Flat, loss of rugae

226
Q

What do you see here, normal is on the left?

A

Flat, loss of rugae

Chronic autoimmune gastritis

227
Q

What do you find in laboratory studies of chronic autoimmune gastritis?

A

Anti-parietal cell and anti-intrinsic factor antibodies

Elevated gastric pH

Elevated serum gastrin

Low vit B12

Megaloblastic anemia

228
Q

What do you see here (this is in the antrum)?

A

Hyperplastig G cells

IN response to chronic autoimmune gastritis

229
Q

What do you see here?

A

ECL cell hyperplasia that can be seen from chronic autoimmune gastritis

230
Q

What can you do to make carcinoid tumors regress?

A

Remove part of the antrum of the stomach - this will allow these carcinoid tumors (typically ECL cell derived) to regress

231
Q

Where does inflammation predominate in response to H. pylori?

A

Antrum

232
Q

What do we see here?

A

H. pylori gastritis

233
Q

What factors does H. pylori secrete?

A

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
Q

What is important about H. pylori’s urease?

A

It not only helps the bacteria neutralize gastric acid, but provides a diagnostic test for its presence

235
Q

What can cause multifocal atrophic gastritis (environmental gastritis)?

A

H. pylori, diet, and other environmental factors

Common in 3rd world countries

10x higher risk for gastric cancer

236
Q

What are etiologies of peptic ulcer disease?

A

H. Pylori and NSAIDs

237
Q

What proportion of stomach ulcers are caused by H pylori vs NSAIDS/other?

A

HP = 70%, rest is other

238
Q

What proportion of duodenal ulcers are caused by H pylori vs NSAIDS/other?

A

HP = 90%, rest is other

239
Q

Where do ulcers arise from MAG?

A

only in stomach

240
Q

Where do ulcers arise from H. pylori?

A

20% in antrum

80% in duodenal bulb

241
Q

When do you see gastric metaplasia of the duodenum?

A

When acid (or excess acid) reaches the duodenum / peptic duodenal ulcers/ with H. pylori

242
Q

How long do peptic ulcers typically take to heal?

A

~6 weeks - cancer can promote formation of ulcer, so if it takes longer, you may suspect cancer

243
Q

What are some complications of H. pylori?

A

Chronic gastritis

Gastric peptic ulcer

Duodenal peptic ulcer

Gastric cancer

MALT lymphoma

244
Q

What are risk factors for gastric cancer?

A

Dietary - smoked, pickled, and grilled foods

Older age

Genetic factors and Fam Hx

Chronic atrophic gastritis (H. pylori, autimmune, environmental)

245
Q

What regions have higher incidences of gastric cancer?

A

Japan, parts of S. america, parts of china

246
Q

What are the two types of gastric cancer?

A

Intestinal - relationship to intestinal metaplasia

Diffuse - describes how the cancer spreads

247
Q

Which type of gastric cancer affects males more than females?

A

“intestinal”

248
Q

Which type of gastric cancer affects females more than males?

A

“diffuse”

249
Q

Which gastric cancer forms a discrete mass?

A

“intestinal”

250
Q

Which gastric cancer has ill-defined gross morphology?

A

“diffuse”

251
Q

Histologically, what do intestinal type gastic cancers look like?

A

Adenocarcinoma - discrete mass, gland formations

252
Q

How does the intestinal type gastric cancer progress?

A
253
Q

What is Linitis Plastica?

A

Rigid, rock-hard thickened stomach

254
Q

What do you see here?

A

Signet ring cells - indicative of adenocarcinoma, diffuse type gastric cancer

255
Q

What are krukenberg tumors?

A

Ovarian metastases of gastric cancers

256
Q

What factor gives a favorable prognosis for gastric carcinoma?

A

Early, submucosal carcinoma vs advanced

257
Q

What are the macroscopic folds of the small intestine called?

A

Folds of Kerkring (plicae circularis)

258
Q

What is the ratio of the villus:crypt heights?

A

4-5:1

259
Q

What are the two predominant epithelial cells of the small intestine?

A

Goblet cells

Columnar cels (enterocytes)

260
Q

Where do epithelial cells of the small intestine originate?

A

Crypt cells - differentiate and migrate up towards villus

Process takes 5-6 days

261
Q

What are paneth cells?

A

At the bottom of the crypt

Elaborate enzymes (lysozyme and defensin)

Help protect progenitor cells from damage

262
Q

Where are paneth cells found?

A

Small intestine

263
Q

What do we see here?

A

A villus of the small intestine

Note the brush border and the lamina propria

264
Q

How much fluid is presented to the small intestine every day?

A

8 L

2 from oral intake, the rest is secretions (salivary, gastric, biliary and pancreatic)

265
Q

How much fluid is presented to the colon?

A

1.5 L (after the small intestine absorbs a lot of fluid and secretes its own)

266
Q

How how much fluid is absorbed by the small intestine?

A

~12 L

267
Q

What percentage of fluid does the small intestine absorb?

A

75-80% (colon is >90%)

268
Q

What is the maximum absorption capacity of the small intestine?

A

12 L / day (more than that => diarrhea)

269
Q

What is the maximum absorption capacity of the colon?

A

5L (more than that => diarrhea)

270
Q

What is the consequence of colonic water reabsorption being a saturable process?

A

Diarrhea if you can’t absorb all you provide

271
Q

What differences do we see between the mucosal epithelium of the small intestine in fasting vs absorptive states?

A

Fasting = cells packed close together; absorptive = potential space is filled

272
Q

How does water get absorbed in the small intestine?

A
273
Q

What are differences between the jejuum, ileum and colon with respect to the permeability of the epithelium?

A

Jejunum allows largest things through, colon smallest

274
Q

What area of the intestines has the highest passive permeability? which has lowest? which has intermediate?

A
275
Q

How does the net water movement change along the course of the intestine?

A
276
Q

What are the three ways that sodium is transported?

A

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
Q

How does electrogenic sodium absorption work?

A

Relies on Na-K ATPase on basolateral membrane

278
Q

How does nutrient-coupled sodium transport work?

A

Can get sodium in if you have glucose to go with it

Also relies on Na-K ATPase basolaterally

279
Q

What is the basis of oral rehydration therapy?

A

Addition of glucose in the lumen to help bring sodium into the body (water follows)

280
Q

How does sodium-hydrogen exchange and sodium chloride absorption work?

A

Also important in acid-base balance

281
Q

What factors can stimulate sodium absorption?

A

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
Q

What is the major ion that drives fluid secretion in the small intestine?

A

Chloride (Cl)

283
Q

How does chloride tranpsort occur?

A

Cl enters basolaterally (Na:K:2Cl transporter), exceeds electrochemical equilibrium, and exits via apical membrane via Cl channel (CFTR)

284
Q

What factors can increase chloride secretion?

A

Hormones

Neural input

Inflammatory factors

Infectious factors

Toxins,

etc

All work by activating cAMP, cGMP, and intracellular calcium

285
Q

What transporter gets chloride from the blood stream into the enterocytes?

A

Na:K:2Cl transporter

286
Q

What channel helps secrete chloride into the lumen of the intestines from the enterocytes?

A

CFTR (chloride channel)

287
Q

What are some factors that increase/decrease transit time?

A
288
Q

What does “diarrhea” mean when a patient says it?

A

Can be:

More frequent stools

Larger volume stools

Looser stools

289
Q

What does diarrhea mean clinically, as a sign?

A

Stool weight > 150-200 g/24 hours

Stool water > 150-200 ml/24 hours

290
Q

What defines acute vs chronic diarrhea?

A

<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
Q

What do large-volume diarrhea indicate?

A

Small intestinal dysfunction

292
Q

What do you see in small intestinal dysfunction wrt stools?

A

Large large volume

293
Q

What do you see in colonic dysfunction wrt stools?

A

Large, but not huge volumes

294
Q

What are some characteristics of small bowel and colonic dysfunction?

A

Large stool volume

Moderate increase in number

Minimal urgency

No tenesmus

Little mucus

295
Q

What are some characteristics of recto-sigmoid dysfunction?

A

Small amount of stool

Frequency

Urgency

Tenesmus

Mucus

Blood

296
Q

What can differentiate small bowel and colonic from recto-sigmoid dysfunction?

A
297
Q

What is the effect of bile acid in your colon?

A

Bile acids induce secretion - ileum is only site of active bile acid absorption

298
Q

What is osmotic diarrhea?

A

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
Q

What are some solutes that can cause osmotic diarrhea?

A

Lactose

Sorbitol (chewing gum), and other sugar substitutes

Na Sulfate lavage solutions

Magnesium citrate

You do this as prep for colonoscopy

300
Q

Why is osmotic diarrhea not life threatening?

A

You lose only water, not sodium - so you maintain your intravascular oncotic pressure

301
Q

What happens in osmotic diarrhea when you decrease intake of the agent?

A

Stool volume decreases

302
Q

What is secretory diarrhea?

A

Stimulation of normal secretory process

Absorptive processes are intact but overwhelmed

303
Q

What things can cause secretory diarrhea?

A

Secretagogues that increase cAMP, cGMP, and/or calcium

Bacterial toxins, hormones, bile acids, drugs, inflammatory mediators

304
Q

How does cholera toxin work?

A
305
Q

What is the effect of fasting on secretory diarrhea?

A

No effect

306
Q

Is secretory diarrhea life threatening?

A

YES - salt and water depletion

307
Q

What is motility diarrhea?

A

Hypermotility - insufficient contact time for absorption (hyperthyroid, cholinergics, laxatives, anxiety)

Hypomotility - stasis and bacterial overgrowth can promote diarrhea

308
Q

What is digestion?

A

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
Q

What is absorption?

A

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
Q

What is this?

A

Intestinal epithelium

311
Q

Where is iron absorbed??

A

Duodenum

312
Q

Where do you absorb you minerals (Ca, Mg, etc)?

A

duodenum

313
Q

Where do you absorb cobalamin?

A

Ileum

314
Q

Where do you primarily absorb bile acids?

A

ileum

315
Q

Where do you absorb carbohydrates?

A

All along small intestine

316
Q

Where do you absorb protein, lipids, sodium, and water?

A

All along the small intestine

317
Q

What is the function of secretin?

A

Hormone - via blood, tells pancreas to tell pancreas to make bicarbonate rich secretion

Slows gastric emptying too

318
Q

What is the result of fatty acids and amino acids reaching the duodenum?

A

CCK production - gallbladder contracts, and tells pancreas to secrete enzymes

319
Q

How are carbohydrates digested?

A

Must be hydrolyzed to monosaccharides

320
Q

What is starch?

A

Polymer of glucose

321
Q

What breaks down starcH/

A

amylase - converts them into smaller glucose units

322
Q

What does maltase do?

A

Breaks down disaccharides to monosaccharides (intestine BBM)

323
Q

Where is amylase found?

A

pancreas, saliva

324
Q

What is sucrose-isomaltase?

A

Fouond on the intestine BBM and converts sucrose to glucose and fructose (disaccharidase)

325
Q

What is lactase?

A

Converts lactase to glucose and galactose (foudn in BBM)

326
Q

How is sucrose digested?

A

Sucrose-isomaltase

327
Q

How is lactose digested?

A

lactase

328
Q

How are carbohydrates absorbed/

A

As glucose/galactose

Actively transported into cell, and then diffuse into portal vein

329
Q

What happens to any unabsorbed carbohydrates?

A

Converted to short chain fatty acids in the colon

Bacteria may also consume it and produce gas

330
Q

What is the schema of carbohydrate digestion?

A

Then

331
Q

What is the schema of carbohydrate digestion product absorption?

A
332
Q

How are proteins digested?

A

Hydrolyzed to oligopeptides or amino acids (4 or 5 aa max)

333
Q

How are proteins digested in the stomach?

A

HCl denatures protein

Pepsin hydrolyzes protein into polypeptides

334
Q

How are proteins digested in the duodenum and pancreas?

A

Pancreas releases proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)

Enterokinase in duodenal BBM activates trypsin which then activates other pancreatic pro enzymes

335
Q

How are proteins digested in the small intestine?

A

BBM oligopeptidases hydrolyze oligopeptides into di- tri- and tetrapeptides and amino acids

336
Q

How are proteins digestion products absorbed?

A

Amino acids and oligopeptides are absorbed and transported inot capillaries (portal vein)

337
Q

Schema for stomach digestion of proteins

A
338
Q

What is the role of the pancreas and duodenum in protein digestion?

A

Pancreatic zymogens are converted inot active enzymes in the duodenum

339
Q

What is the schema of absorption of amino acids and short peptides in the small intestine?

A
340
Q

How are lipids digested?

A

Emulsification, lipolysis, micelles

341
Q

What is the role of the stomach in lipid digestion?

A

Churns fat into an unstable emulsion

342
Q

What is the role of the duodenum and small intestine in lipid digestion?

A

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
Q

What is the role of pancreatic lipase and co-lipase in lipid digestion?

A

Converts triglycerides into monoglycerides and free fatty acids

344
Q

How are lipid digestion products absorbed?

A

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
Q

Where in the circulation do lipids go once digested?

A

Long chain triglycerides go to the lymphatics (most)

Medium chain triglycerides go to the portal vein

346
Q

What is teh schema for stomach digestion of lipids?

A

lipolysis is very little - mostly emulsification

347
Q

What is the schema for fat digestion in the small intestine?

A


348
Q

What is the schema for lipid product absorption?

A
349
Q

What is the schema for lipid product absorption and entrance to the circulation?

A
350
Q

How is vitamin B12 absorbed?

A

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
Q

What is the clinical finding you see when you malabsorb protein?

A

edema

352
Q

What is the clinical finding you see when you malabsorb fat?

A

steatorrhea, weight loss

353
Q

What is the clinical finding you see when you malabsorb carbohydrates?

A

diarrhea, bloating, gas

354
Q

What is the clinical finding you see when you malabsorb vit. A?

A

night blindness, hyperkeratosis

355
Q

What is the clinical finding you see when you malabsorb vit D., calcium?

A

tetany (muscle spasms/involuntary contractions), osteomalacia

356
Q

What is the clinical finding you see when you malabsorb vitamin E?

A

Neuropathy

357
Q

What is the clinical finding you see when you malabsorb vit. K?

A

Ecchymoses

Bruising

358
Q

What is the clinical finding you see when you malabsorb vit B12?

A

Megaloblastic anemia

Glossitis

Cheilosis

Neuropathy

359
Q

What is the clinical finding you see when you malabsorb Folate?

A

Megaloblastic anemia

Glossitis

360
Q

What is the clinical finding you see when you malabsorb iron?

A

Microcytic anemia

Dyspnea

Fatigue

Glossitis

361
Q

Which regions commonly get primary lactase deficiency?

A

Asians, Africans, Mediterranean descent

362
Q

What can cause secondary lactase deficiency?

A

Loss of enterocytes (infection, resection, radiation)

363
Q

What are symptoms of lactase deficiency?

A

Diarrhea, gas, bloating, borborygmi (stomch grumblings)

364
Q

What are ways to diagnose lactase deficiency?

A

Good history

Hydrogen breath test if needed

365
Q

How does a hydrogen breath test work?

A

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
Q

What is the treatment for lactase deficiency?

A

Avoid dairy

Exogenous lactase

Lactose-free products

367
Q

What is the schema for lactase deficiency?

A
368
Q

What is the result of pancreatic exocrine insufficiency?

A

Fat, protein, carbohydrates are all maldigested

369
Q

How much pancreatic function must be lost before you get pancreatic exocrine insufficiency?

A

90-95% of the pancreatic function

370
Q

What are some examples of things that may cause pancreatic exocrine insufficiency?

A

Cystic fibrosis (in children)

Chronic pancreatitis

Pancreatic resection

371
Q

How do you diagnose pancreatic exocrine insufficiency?

A

Usually on x-ray due to calcifications from scarring (or on CT)

372
Q

How do you treat patients with pancreatic exocrine insufficiency?

A

Oral pancreatic enzyme replacement

Enteric coated (with acid suppressing agent)

373
Q

What do you see in patients with bile salt deficiency?

A

Difficulty digesting fat/fat-soluble vitamins

374
Q

What are examples of things that can causebile salt deficiencies?

A

Severe cholestasis

Distal ileal resection or disease (Crohn’s) - where it is reabsorbed

Bacterial overgrowth - bacteria make bile salts unusable

375
Q

How do you diagnose bile salt deficiency?

A

Work-up of underlying disease

376
Q

How do you treat bile salt deficiency?

A

Treat underlying condition

Feed medium chain triglycerides instead

377
Q

What are factors that protect against bacterial overgrowth?

A

Gastric acid

Small bowel motility

Ileocecal valve

Secreted immunoglobulins

378
Q

What can cause bacterial overgrowths?

A

Poor motility

Decreased gastric acid

Connection between colon and small intestine (no ileocecal valve, perhaps, or fistula)

Few immunoglobulins

379
Q

What are some conditions associated with bacterial overgrowth?

A

Motility disorders (stasis)

Anatomic disorders (fistula, diverticula, blind loop)

380
Q

What are some consequences of bacterial overgrowth?

A

Fat malabsorption: bacteria conjugate/dehydroxylate bile salts

Vit. B12 deficiency - they consume vit. B12

381
Q

How can you diagnose bacterial overgrowth?

A

Schilling test, breath test

382
Q

How do you treat bacterial overgrowth?

A

Correct underlying problem; antibiotics

383
Q

What can cause short bowel syndrome?

A

Resection (due to chrohn’s, infarct, radiation, trauma, cancer)

Bypass (surgical, fistula)

384
Q

What happens if you lose your first 100cm of jejunum?

A

It is responsible for >90% of digestion/absorption

385
Q

What happens if you lose your last 100 cm of terminal ileum?

A

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
Q

How do you diagnose a short bowel syndrome?

A

Small bowel imaging (CT/ MRI)

387
Q

How do you treat short bowel syndrome?

A

Enteral feeding if possible

Total parenteral nutrition

Small intestine transplant

388
Q

What is celiac disease?

A

Inappropriate immune response to gliadin (a protein in gluten)

Common in northern European population

389
Q

What occurs histologically in celiac disease?

A

Villous atrophy

Crypt hyperplasia

Plasma cells in lamina propria

Intraepithelial lymphocytes (IELs)

390
Q

Where along the GI tract does celiac disease affect most?

A

Proximal more than distal small intestine (thats where the gliadin first hits)

391
Q

What are immunological abnormalities seen in celiac disease?

A

HLA-DQ2, DQ8

selective IgA deficiency, diabetes, autoantibodies

392
Q

What are some associations/complications with celiac disease?

A

Dermatitis herpetiformis (skin rash)

Collagenous sprue

T cell lymphoma

393
Q

How do you diagnose celiac disease?

A

Small bowel biopsy pre and post diet

Autoantibodies

394
Q

How do you treat celiac disease?

A

Eat a gluten-free diet

395
Q

What do you see here?

A

Active Celiac sprue

Villous atrophy

Crypt hyperpasia

Inflammation of lamina propria

396
Q

What is tropical sprue?

A

Acquired syndrome - some bug yet unidentified

Affects entire small bowel (proximal and distal)

Similar to celiac

397
Q

What is the difference in location of disease in tropical sprue and celiac sprue?

A

Tropical is all throughout small bowel

Celiac is more proximal

398
Q

What are differences between tropical and celiac sprue?

A
399
Q

What is abetalipoproteinemia?

A

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
Q

What is this?

A

Abetalipoproteinemia

401
Q

How do you diagnose abetalipoproteinemia?

A

Small bowel biopsy

402
Q

How do you treat abetalipoproteinemia?

A

Dietary fat restriction

Medium chain triglyceride oil

403
Q

How do you test for malabsorption?

A

Blood tests and specialized tests

404
Q

What can a CBC show malabsorption for?

A

Anemia - micro or macrocytic

405
Q

What does microcytic anemia indicate?

A

Iron deficiency (malabsorption)

406
Q

What does macrocytic anemia indicate?

A

B12 or Folate deficiency

407
Q

What does low albumin indicate?

A

Protein malabsorption

408
Q

What does low calcium indicate?

A

Vit. D or calcium malabsoroption (duodenal disease)

409
Q

What does prolonged prothrombin time indicate?

A

Vitamin K deficiency or malabsorption -> fat absopriton issue (vit. A, D, E, K)

410
Q

What is a fecal fat analysis useful for?

A

Quantify steatorrhea - to identify pancreatic disease

411
Q

What does a D-xylose test help identify?

A

Small bowel disease

412
Q

How does a D-xylose test work?

A

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
Q

How do you workup fat malabsorption?

A

72 hour fecal fat followed by D-xylose test if abnormal

414
Q

What is Meckel’s Diverticulum?

A

Most common congenital anomaly of the GI tract

Outpouching of the small intestine from failure of vitelline duct closing

415
Q

What is this?

A

Meckel’s Diverticulum

416
Q

Where is Meckel’s Diverticulum located?

A

2 feet from the colon and close to the appendix grossly

417
Q

What are the two most common heterotopic tissues seen with Meckel’s Diverticulum?

A

gastric -> peptic ulcer

pancreatic -> not many symptoms

418
Q

How do you perform a Meckel’s Scan?

A

Tectecium - seen in stomach - also can be seen in Meckel’s Diverticulum if you have heterotopic tissue excreting acid

419
Q

What are problems with extrinsic obstructions of the small intestine?

A

Intestinal ischemia - requires multiple blood vessels to be obstructed or flow from SMA

420
Q

Why is the small intestine susceptible to esxtrinsic mechanical obstruction?

A

Pliant wall

Narrow lumen

Long length

421
Q

Why is it difficult to get intestinal ischemia of the small intestine (and why is it a problem if you do get it)?

A

Many collateral circulations

Ischemia means that either SMA flow is compromised or multiple blood vessels are compromised

422
Q

What are sources of extrinsic obstruction of the bowel that can cut off multiple blood vessels?

A

Strangulated hernia

Volvulus

Intussusception

423
Q

What do extrinsic obstructions of the small intestine have in common?

A

Distended

Reddish necrotic color

Exudate often seen

e.g.

424
Q

What is a hernia?

A

Weakness in peritoneum- intestines pouch out

Typically reducible (can be pushed back)

Can compress veins and arteries (can cause extrinsic obstruction)

425
Q

What is volvulus?

A

Bowel twisted upon itself

426
Q

What are risk factors for volvulus?

A

Adhesions (after surgery, or congenitally, for example)

Poor motility (diabetics, neurologic diseases)

Abnormal mesentery

Congenital malrotation

427
Q

What is intussusception?

A

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
Q

What is the common cause of intussusception in adults?

A

Benign or malignant tumor - surgery removes it

429
Q

What is the common cause of intussusception in children?

A

Hyperplastic lymphoid tissue - treat with retrograde barium enema to reverse intussusception

430
Q

What causes intussusception?

A

Mass lesion as leading point (children = lymphoid tissue; adults = tumors)

431
Q

What is gluten sensitive enteropathy?

A

Celiac disease

432
Q

What is the protein that is the source of celiac disease?

A

Gliadin - in gluten

433
Q

What is an inflammatory disease triggered and maintained by exposure to gliadin?

A

Celiac disease

434
Q

Approximately how many north americans have celiac disease?

A

0.111111111

435
Q

How many celiac disease patients are symptomatic?

A

20%

436
Q

What are the two implicated HLA types in celiac disease?

A

95% HLA-DQ2

5% HLA-DQ8

437
Q

What is an important serum marker for Celiac Disease?

A

Circulating IgA antitissue transglutaminase (TGT)

Indicator of active disease too

438
Q

When does Celicac Disease typically onset?

A

At any age

At infancy you are exposed to cereals

439
Q

What are symptoms of celiac disease?

A

Steatorrhea

Failure to thrive

Short stature

Calcium malabsorption, osteoporosis - proximal small bowel absorbs nutrients

Iron-deficiency anemia - proximal small bowel absorbs nutrients

Infertility

440
Q

Disease progression from normal on left to severe on right. What disease is this?

A

Celiac Disease

Partial then total villous atrophy

441
Q

What can be found in the surface epithelium in Celiac Disease?

A

Intraepithelial lymphocytes

442
Q

What do we see here?

A

Intraepithelial lymphocytes characteristic of Celiac Disease

443
Q

What finding do you see in the crypts in Celiac Disease?

A

Increased crypt mitoses

444
Q

What finding do you see here?

A

Increased crypt mitoses - Celiac Disease

445
Q

What histological finding do you see in the lamina propria in Celiac Disease?

A

Chronic inflammation

446
Q

What is this finding?

A

Chronic inflammation in Celiac Disease

447
Q

What factor correlates with the severity of malabsorption in Celiac Disease?

A

Severity of villous atrophy

448
Q

What factors go into the diarrhea seen in Celiac Disease?

A

Attenuated glycocalyx -> impaired digestion; lactase deficiency

Attenuated microvilli -> attenuated absorption

Damaged organelles -> impaired metabolism and absorption

449
Q

What are some diseases associated with Celiac Disease?

A

Ulcerative jejunoileitis

Enteropathy-associated T cell lymphoma

GI & non-GI cancers

Dermatitis Herpetiformis

Collagenous sprue

450
Q

What is Whipple’s Disease?

A

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
Q

What organism causes Whipple’s DIsease?

A

Trophyrema whipplei

452
Q

What is Trophyrema whipplei?

A

Intracellular bacillus related to M. avium that causes Whipple’s Disease

453
Q

What is the treatment for Whipple’s Disease?

A

Antibiotics - caused by Trophyrema whipplei

454
Q

What is the diagnostic test for Whipple’s Disease?

A

PCR for Trophyrema whipplei

455
Q

What causes obstruction in the case of Whipple’s Disease?

A

Lymphatic obstruction due to bacterial infection

456
Q

What is Congenital Lymphangiectasia?

A

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
Q

What are some symptoms of congenital lymphangiectasia?

A

Asymmetrical edema

Chylous ascites

Malnutrition, lymphocytopenia, recurrent infections

458
Q

What gene causes Congenital lymphangiectasia?

A

VEGFR-3

459
Q

What is a danger of small intestinal diverticuli?

A

Bacterial overgrowth

460
Q

What is this?

A

Small intestinal diverticulosis

Can cause bacterial overgrowth and lead to malnutrition

461
Q

What is a true diverticulum?

A

All layers of intestinal wall present

462
Q

What is a false diverticulum?

A

Mucosa only

463
Q

What is the only true diverticuluM?

A

Congenital - e.g. Meckel’s

464
Q

What history items are crucial for a nutritional assessment?

A

Weight loss

Food intake

Malabsorption

Micronutrient deficiencies

465
Q

What physical exam markers are important for a nutritional assesment?

A

Weight/BMI

Anthropometrics

Tissue depletion

Hydration status

466
Q

What are important laboratory markers of nutritional assessment?

A

Albumin

Transferrin

Transthyretin

467
Q

What does mild/moderate malnutrition look like?

A

BMI 16-18.5

Weight loss of 5-10%

Functional Impairment

468
Q

What does severe malnutrition look like?

A

BMI < 16

Weight loss > 10%

Muscle Wasting

Functional Impairment

469
Q

What are the three ways we expend energy?

A

Resting energy expenditure (REE) - 70%

Energy expenditure of physical activity - 20%

Thermic effect of feeding - 10%

470
Q

What is a normal intake for a healthy adult?

A

20-25 kcal/kg

471
Q

What are the three sources of energy in a western diet?

A

Protein 10-15% (4cal/g)

Carbohydrates 55% (4cal/g)

Fats 30% (9cal/g)

472
Q

What is the most energy rich food?

A

Fats (9cal/g)

473
Q

What are micronutrients?

A

Don’t give energy, but crucial

Vitamins (Fat and water soluble) and minerals

474
Q

What are macronutrients?

A

Give energy

Protein, carbohydrates, fats

475
Q

What is primary protein energy malnutrition?

A

Inadequate nutrient intake (may be due to a variety of things)

476
Q

What is secondary protein energy malnutrition?

A

Elevated requirements in the face of illness/injury with relative inadequate intake (not necessarily an intake problem)

477
Q

What is kwashiokor?

A

Protein malnutrition

Presents with edema, lethargy, low serum albumin

478
Q

What is protein malnutrition with edema, lethargy, and low serum albumin known as?

A

Kwashiokor

479
Q

What is marasmus??

A

Total malnutrition

With weight loss, muscle mass and subcutaneous fat loss and normal serum albumin

480
Q

What malnutrition is of all macronutrients, presents with weight loss, muscle and subcutaneous fat loss and with normal serum albumin?

A

Marasmus

481
Q

When do you provide nutrition support?

A

Acutely Ill

Moderate-Severe malnutrition

Unable to meet nutritional needs within 48 hours

Malnourished and need major surgery

482
Q

What BMI defines “underweight”

A

<18.5

483
Q

What BMI range is normal?

A

18.5 - 24.9

484
Q

What BMI defines “overweight”?

A

25-29.5

485
Q

What defines Class I obesity?

A

30-34.9

486
Q

WHat defines Class II Obesity?

A

35-39.5

487
Q

What defines Class III obesity?

A

>40

488
Q

How do you assess obesity in pediatric patients?

A

By BMI percentile

489
Q

What are some genetic causes of obesity?

A

Prader-Willi, Bardet Biedl, Leptin deficiency

Very rare

490
Q

What are medical conditions that can lead to obestiy?

A

Cushings Syndrome

Hypothyroid

Hypothalamic Injury

Rare

491
Q

What are environmental factors that can cause obesity?

A

Smoking cessation

Post pregnancy

Sleep deficiency

492
Q

What are the brakes in feeding?

A

POMC and CART make α-MSH to stop hunger

493
Q

Where is leptin produced?

A

Adipose tissue

494
Q

What ist he target of leptin?

A

Hypothalamus

495
Q

What is the action of leptin?

A

Decrease energy intake

GI and Liver (3 decks)

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