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Pathophys > GI Pathophys > Flashcards

GI Pathophys Flashcards

1
Q

what is a inlet patch

A

most common type of ectopic tissue. It is a patch of gastric mucosa in the upper 1/3 of esophagus. Can result in dysphagia, esophagitis, Barrett esophagus or rarely adenocarcinoma

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2
Q

what is ectopic pancreatic tissue

A

Found in esophagus or stomach.

Asymptomatic

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3
Q

what is gastric heterotopia

A

ectopic gastric mucosa in small bowel or colon

Can results in peptic ulceration of adjacent mucosa

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4
Q

why causes Barrett esophagus and why does it need to be monitored

A

GERD causes acid in esophagus= metaplasia into gastromucosal cells to protect the esophagus by secreting mucos. The metaplasia can transform it into adenocarcinoma.

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5
Q

how does gastric heterotopia cause peptic ulceration

A

acid is secreted into the colon or duodenum which do not have mucus producing cells to protect it

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6
Q

what are congenital duplication cysts and where are they usually located

A

they form double smooth muscle layers by replicating normal anatomy of affected tissue.
Usually located in small bowel(50%), esophagus, and colon

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7
Q

what are bronchogenic cysts

A

fluid filled lung tissue often present as mediastinal masses lined by bronchial tissue.

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8
Q

what is the treatment for duplication and bronchogenic cysts

A

they usually need to be surgically removed and closed off

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9
Q

what is associated with increased risk of esophageal atresia

A

polyhydramnios (excessive amniotic fluid)

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10
Q

if a child has esophageal atresia, what other conditions is this child at inc risk for?

A

VATER(vertebral defects, anal atresia, tracheoesophageal fistula, and renal dysplasia) along with congenital heart defects, genitourinary malformations and neurologic disease

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11
Q

are esophageal webs and rings congenital or acquired

A

can be either (can be acquired from GERD creating fibrotic tissue)

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12
Q

what is the histology of esophageal webs/rings

A

Core of fibrovascular tissue lined with normal esophageal epithelium

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13
Q

what is the manifestation of esoph webs/rings

A

episodic dysphagia

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14
Q

where are schatzki rings located

A

Type A: above the GE junction

Type B: at the squamocolumnar junction

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15
Q

esophageal webs/rings Tx?

A

dilation or excision

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16
Q

What is Plummer-Vinson Syndrome and what can be a severe complication from it

A

Occurs mainly in females causing iron deficiency anemia, esophageal web, mucosal lesions of mouth and pharynx. Can cause carcinoma of oropharynx and upper esophagus

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17
Q

what is the most common manifestation of esophageal stenosis and why is it caused

A

progressive dysphagia from atrophy of the muscularis propria

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18
Q

what causes diaphragmatic hernia and what is its effect

A

Incomplete formation of diaphragm causing

  • Abdominal viscera herniating into thoracic cavity
  • Webs and rings
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19
Q

what is a Omphalocele

A

Closure of abdominal musculature is incomplete

Abdominal viscera herniates into ventral membranous sac

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20
Q

if a baby has a omphalocele, what else are they likely to have

A

40% have other birth defects (diaphragmatic hernia, cardiac abnormalities)

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21
Q

what is gastroschisis

A

bentral wall defect involving all layers of abdominal wall allowing the organs to move out of body w/o any type of membranous casing

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22
Q

what is a Meckel diverticulum

A 
Blind outpouching
Communicates with lumen
All three layers of bowel wall
Rule of 2s
2 feet from iliocecal valve
2% of population
Approx. 2 inches long
Twice as common in males
Symptomatic by age 2 years
2 types of common ectopic tissue:  gastric and pancreatic
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23
Q

what is a true diverticulum

A

blind outpouching of the alimentary tract that is lined by mucosa, communicates with the lumen, and includes all three layers of the bowel wall.

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24
Q

is a pyloric stenosis more common in men or women

A

4:1 men:women

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25
Q

when does pyloric stenosis begin its manifestatioins

A

2nd-3rd weeks of life

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26
Q

what is the genetic etiology of pyloric stenosis

A

nitric oxide synthetase deficiency= hyperplasia of pyloric muscularis propia

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27
Q

what are the Sx of pyloric stenosis

A 
New onset regurgitation(vomiting)
Persistant, projectile, nonbilious
Hypochloremic alkalosis
Physical Exam
Hyperperistalsis
Firm ovoid abdominal mass
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28
Q

how does regurgitation of SBO differ from pyloric stenosis

A

SBO will have bile in it

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29
Q

what does a firm acorn-like mass at the end of the xiphoid indicate

A

pyloric stenosis

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30
Q

what is Hirschsprung Dz (cause and effect)

A

Either normal migration of neural crest cells from cecum to rectum is arrested or ganglion cells undergo premature death= the distal intestinal segment to lacks both Meissner submucosal and Auerbach myenteric plexus= No peristalsis= distended colon

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31
Q

what is the two types of smooth muscle in the esophagus

A

longitudinal

circular

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32
Q

what is the role of the submucosa in the esophagus

A

contains glands that secrete mucus to prevent the esophagus from drying out

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33
Q

what is the role of the connective tissue around the esophagus

A

protection

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34
Q

what is the order of layers in the esophageal wall from inside out

A

squamous epithelium, muscularis mucosa, submucosa, muscularis propria

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35
Q

what are the two main enzymes in saliva and what do they break down

A

Alpha-amylase: break down sugars

lingual lipase: break down fats

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36
Q

what nerve controls chewing and where does it originate from

A

trigeminal- originates at the pons

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37
Q

what is trigeminal neuralgia

A

hyperactive afferent= inc pain with mastication

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38
Q

what are the 3 stages of swallowing

A

1-Voluntary - initiates swallowing process
2-Pharyngeal - passage of food through pharynx into esophagus
3-Esophageal - passage of food from pharynx to stomach

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39
Q

what nerves are involved in swallowing

A

Mainly CN 9 and 10. Some trigeminal in mouth

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40
Q

how do you test if there is damage to the medullary region of the brain stem

A

CN 9 and 10 can be tested by the gag reflex

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41
Q

what is the neural pathway when a bolus of food reaches the pharynx

A

it is sensed in the pharynx by CN 9/10 afferent. This is transmitted to the swallowing center in the medulla. Efferent n then go out to contract/relax the glottis/ epiglottis

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42
Q

what inhibitory effect does the swallowing center have

A

inhibits the respiratory center when swallowing

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43
Q

what is primary peristalsis

A

it is cordinated by the swallowing center and is a continuation of pharyngeal peristalsis moving bolus downward

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44
Q

what is secondary peristalsis

A

it only occurs when needed and is induced by distention of the esophagus. It repeats until the bolus is cleared

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45
Q

what is unique about the striated muscle in the upper esophagus

A

The striated and smooth muscle of the esophagus are both innervated by the vagus nerve. Striated muscle is normally innervated by motor neurons

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46
Q

can primary and secondary peristalsis occur after a vagotomy or stroke damage to the vagus nerve

A

primary cant, secondary can

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47
Q

when is a vagotomy indicated

A

not used often but it can dec acid production and dec spasms

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48
Q

what are the esophageal pressure measurements between swallows

A

High pressure at sphincters

Pressure in esophageal body = intrapleural pressure

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49
Q

what are the esophageal pressure measurements during swallowing

A

UES relaxes - (low pressure)
Peristaltic wave - (high pressure)
LES and fundus relax - receptive relaxation (low pressure).

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50
Q

to continue a peristaltic wave, what is released at the level of the bolus

A

Ach and SP (substance P) to initiate contraction

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51
Q

to continue a peristaltic wave, what is released inferior to the bolus. Also what nerve causes this

A

NO/ VIP/ATP to cause relaxation distal to the bolus. This is caused by vagal input to the nonadrenergic/ noncholenergic receptors

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52
Q

What is the purpose of high resting pressures in the UES and LES

A

UES - keeps air from entering esophagus

LES - prevents acid reflux into esophagus

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53
Q

how can a stroke cause aspiration

A

UES and pharyngeal contractions are not coordinated

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54
Q

how do myasthenia gravis and polio affect swallowing

A

both destroy Ach receptors= diff swallowing

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55
Q

how does botulism affect swallowing

A

blocks Ach release= diff swallowing

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56
Q

what is the nutcracker esophagus

A

“steakhouse esophagus”

Lack of coordination between longitudinal and circular smooth muscle contraction which can lead to obstruction from bolus

57
Q

what is a diffuse esophageal spasm and what can it lead to

A

Functional obstruction

Can lead to diverticulae in esophagus

58
Q

what is Zenker diverticulum

A

located above the UES

59
Q

what is a traction diverticulum

A

located near the midpoint of esoph

60
Q

what is a epiphrenic diverticulum

A

immediatly above LES

61
Q

what is patterson brown kelly syndrome

A

AKA Plummer-Vinson syndrome

assoicated with iron deficiency anemia, glossitis, and cheilosis

62
Q

what is the size of the protrusions from esophageal webs

A

protrude less than 5mm with thickness of 2-4 mm

63
Q

what are schatzki rings

A

circumferential esophageal rings

64
Q

what are type A and B schatzki rings

A

A rings: distal esophagus above gastroesophageal junction
Covered by squamous mucosa
B rings: located at squamocolumnar junction of lower esophagus. Have gastric type mucosa

65
Q

achalasia is caused by what triad

A

Incomplete LES relaxation
Increased LES tone
Aperistalsis of esophagus
causing Food retained in esophagus and Organ hypertrophies and dilates

66
Q

what causes primary achalasia

A

failure of distal inhibitory neurons

Other causes: degenerative changes(DM, ETOH) in neural innervation(vagus)

67
Q

what is Chagas Dz

A

Trypanosoma cruzi infection which destroys myenteric plexus= dec parastolsis

68
Q

what are complications of hiatal hernias

A

ulcerations, obstruction

69
Q

what is the Mallory-Weiss syndrome

A

Longitudinal tears at GE junction due to severe retching or vomiting
May involve only mucosa or may penetrate deeply and perforate the wall

70
Q

what type of pts is Mallory-Weiss syndrome more often seen in

A

bolemic, ETOH abuse

71
Q

where are the lacerations from Mallory-Weiss syndrome usually located

A

Usually cross gastroesophageal junction and in proximal gastric mucosa

72
Q

what is Boerhaave syndrome:

A

distal esophageal rupture

rare but catastrophic

73
Q

what are the Sx of esophagitis

A

Retrosternal pain, dysphagia, odynophagia

74
Q

what causes esophagits

A

Reactive: GERD
Infectious: Candida, Herpes, CMV
Toxic: Pill, Ulcer, Alkali or Acid Ingestion
Other: radiation, GVH

75
Q

what is the pathology causing esophagitis

A

Inflammatory cells (eosinophils, neutrophils or lymphocytes) within the epithelium and lamina propria

76
Q

what cells are likely to be the cause of esophagitis in 1)acute infection 2)allergic/ parasitic 3)chronic infection 4)yeast/ viral

A

1) acute infection = inc neutrophils
2) allergic/ parasitic =inc eosinophils
3) chronic infection = inc lymphocytes
4) yeast/ viral = inc lymphocytes

77
Q

what are likely findings on a pathology report from acute esophagitis

A

Numerous neutrophils in the epithelium

Reactive squamous cells

78
Q

what are likely findings on a pathology report from chronic esophagitis

A

Inflamed lamina propria with inc lymphocytes and inc monocytes

79
Q

what are punched out ulcers seen with

A

herpes esophagitits

80
Q

what is the pathophysiology causing GERD

A

dec in LES tone or inc abd pressure(ETOH, smoking, obesity, Pg) causing…
Inflammatory response (eosinophils and lymphocytes within the mucosa)
Basal zone hyperplasia
Elongation of lamina propria papillae into the top 1/3 of the epithelium with capillary congestion
Squamous cells react – mucosa may ulcerate and bleed – may undergo metaplasia

81
Q

what is eosinophilic esophagitis

A

“Increased intraepithelial eosinophils in the esophagus”

First described in children; incidence appears to be increasing in adults (especially in young men)

82
Q

what are the Sx of eosinophilic esophagitis

A

Longstanding dysphagia with solid foods
Food impaction
GERD Sx without improvement on therapy(proton pump inhibitors, etc)

83
Q

what will endoscopy show if eosinophilic esophagitis is present

A

Small caliber esophagus
Corrugated (ringed) esophagus
Proximal esophageal stenosis

84
Q

eosinophilic esophagitis

A

Dietary change
Steroids
Montelukast

85
Q

what will a micro report show if eosinophilic esophagitis

A

Numerous intraepithelial eosinophils, often forming eosinophilic “microabscesses”

86
Q

what differentiates eosinophilic esophagitis from GERD

A

Failure of proton pump inhibitor treatment and absence of acid reflux is necessary for diagnosis.
Also, EE is Present in proximal and distal esophagus (a biopsy from the proximal esophagus is needed to exclude GERD)

87
Q

who is most likely to get Barrett’s Esophagus

A

middle aged to older white men

88
Q

what is a complication of longstanding GERD

A

Chronic mucosal injury causes the squamous mucosa to change into intestinal-type mucosa with goblet cells (“intestinal metaplasia” / “specialized metaplasia”)

89
Q

what is the management for Barretts esophagus

A

BE without dysplasia: 1yr then at 3yr intervals

BE with low grade dysplasia: 1 yr intervals until negative for dysplasia

BE with high grade dysplasia: Although HGD is not cancer, there is a high likelihood that there may be cancer elsewhere in the Barrett’s segment
Aggressive surveillance every 3 months
Resection (Esophagectomy)
Ablation/Endomucosal resection

90
Q

what is the Tx for Barretts esophagus with “intramucosal adenocarcinoma”

A

Since lymphatics are present within the mucosa, treat aggressively: esophagectomy or Ablation/Endomucosal resection

91
Q

what do esophageal varices result from

A

Dilated submucosal veins due to portal hypertension(Fibrotic liver) and shunting of blood from the portal to systemic venous system (collateral circulation)

92
Q

esophageal varices buldge inward, what risk does this present

A

tearing from food, ulceration

93
Q

how severe is ruptured esophageal varices

A

50% die from 1st bleeding episode

94
Q

what are the three types of cells esophageal tumors are derived from and what type of tumors are they

A

squamous epithelium (squamous cell carcinoma and squamous papiloma)

glandular epithelium (adenocarcinoma)

the muscular wall (leiomyoma)

95
Q

what is the most common benign tumor of the esophagus

A

leiomyoma

96
Q

can leiomyomas be visualized

A

they can be visualized by endoscopy in the esophageal wall

97
Q

what functional problem can occure with leiomyomas

A

they can form a obstruction so they can be removed (do risk reoccurring)

98
Q

what causes squamous papilloma in the esoph

A

HPV

99
Q

what is characteristic of squamous papillomas

A

Hyperplastic papilliform squamous mucosa overlying a fibrovascular core

100
Q

why is the incidence of adenocarcinoma increasing

A

increasing barretts

101
Q

what mutation is associated with SCC

A

p53 tumor suppressor gene

102
Q

where is the most common location of SCC in esoph

A

middle most common but can occur in upper or lower (but lower more likely to be adenocarcinoma

103
Q

what treatment has been known to inc risk for SCC in esoph

A

thoracic cavity radiation

104
Q

what factors are associated with SCC

A 
Alcohol
Tobacco:  increases risk 5 to 10 fold
HPV
Nitrosamines in food (China, S. Africa)
Chemical injury
Polycyclic hydrocarbons-Burnt food
Chronic Fungus= constant inflam
105
Q

what is the lifetime risk of developing adenocarcinoma from barretts

A

around 10% depending on the severity of dysplasia in Barretts

106
Q

what is the process from Barretts becoming adenocarcinoma

A

Normal-inflamed and reactive- low grade dysplasia- high grade dysplasia- invasive adenocarcinoma

107
Q

where does adenocarcinoma typically appear

A

distal esoph

108
Q

what part of the stomach mainly produces mucus

A

fundus and the antrum

109
Q

what types of cells are mainly located in the body of the stomach and what do they secrete

A

chief and parietal cells secrete acid and pepsinogen

110
Q

what effect does increased vagus tone have on the stomach

A 
inc motility
inc secretions(HCl, mucus, pepsinogen)
111
Q

what effect does increased sympathetic tone have on the stomach

A

dec acid
dec motility
dec vascular supply

112
Q

what is the vascular supply of the stomach

A

many different arteries supply the different parts of the stomach. All drain into the portal system which goes to the liver

113
Q

what are characteristic of gastric pits

A

they are shallow pits that rapidly reproduce for replacement. mucus does extend into these for protection

114
Q

where is the lamina propria located and what does it do

A

located under the mucosal muscularis and epithelial cells. It acts as the loose connective tissue of the mucosa

115
Q

what is a oxyntic

A

another term for parietal cells

116
Q

what is the function of parietal cells

A

secrete HCL and intrinsic factor

117
Q

what is the function of intrinsic factor

A

it is produced by the parietal cells and is necessary for the absorption of vit B12

118
Q

what is the function of chief cells(Zymogen)

A

produces pepsiongen 1 which is a zymogen(activated by acid) that digests proteins

119
Q

what are the enteroendocrine cells AKA

A

G cells

120
Q

what is the function of the enteroendocrine cells

A

release Gastrin into the blood stream(endocrine). Not released into the stomach.

121
Q

what is the function of mucus cells

A

secrete mucus and pepsinogen II

122
Q

what is the function of pepsinogen II

A

function not exactly known. They are starting to test pep I/pep II ratio for some GI Dz

123
Q

what is the pathway of stimulating and releasing HCl from the parietal cells

A

1) CO2 combines with H20 with carbonic anhydrase to make carbonic acid.
2) carbonic acid dissociates freely into bicarb and H+.
3) H+ is excreted by a energy dependent proton pump
4) Cl- follows the charge of the H+ leaving

124
Q

are PPIs reversible or irreversible

A

irreversible so the parietal cells will need to create more proton pumps to release the acid

125
Q

what stimulates parietal cells to release HCl

A

ACh- inc carbonic anhydrase and inc production of proton pumps

126
Q

what effect does the vagus nerve have on parietal cells

A

inc Ach release = inc carbonic anhydrase and inc production of proton pumps

127
Q

what stimulates the vagus nerve at the stomach

A

stomach distention

128
Q

what stimulates the parietal cells to release HCl and what meds prevent this.

A

Vagus (Anticholenergics), Gastrin in bloodstream, Histamine (H2 blockers)

129
Q

how do digested proteins inc HCl release

A

gastrin releasing peptides(protein in stomach) activate G cells= inc gastrin in blood stream= directly stimulates parietal cells to release HCl and indirectly stimulate H2 release

130
Q

what is Zollinger ellsion syndrome

A

gastrin releasing tumor= inc HCl release= inc ulcers

131
Q

where are the D cells located

A

antrum and duodenum

132
Q

what is the function of D cells

A

They get stimulated as bolus moves into intestines and release somatostin which inhibit G cells= dec acid release

133
Q

what type of receptor in the parietal cells do anticholenergic meds block so they do not affect the heart

A

muscarinic type 3 (M3)

134
Q

what type of receptors does gastrin bind in the parietal cells

A

cholecyctokinin type 2 receptor (CCK-B)

135
Q

what pathway do ACh and Gastrin both activate in the parietal cells

A

both activate PLC to inc Ca and phosphokinase= provides more energy for the parietal cell to inc HCl release

136
Q

what receptor does Histamine bind on the parietal cells and what is its effect

A

binds H2 receptor= actives the G protein system= inc Camp= activation of protein kinases= physphorylation and inc energy

137
Q

what is prostaglandins effect on the stomach

A

inc mucus production

dec acid production

138
Q

what is somatostatins effect on the stomach

A

binds parietal cells which inhibit G cells= dec acid release

Pathophys (15 decks)

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