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Health Assessment > GI Disorders - Exam IV > Flashcards

GI Disorders - Exam IV Flashcards

1
Q

The GI tract constitutes ____ of the total human body mass

A

5%

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2
Q

What are the main functions of the GI tract?

A
  1. motility
  2. digestion
  3. absorption
  4. excretion
  5. circulation
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3
Q

Outermost to innermost layers of the GI tract

A

serosa - longitudinal muscle layer - circular muscle layer - submucosa - mucosa

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4
Q

Mucosa layers (outermost to innermost)

A

muscarlis mucosae, lamina propria, epithelium

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5
Q

The ____ is a smooth membrane of thin connective tissue and cells.

What does it do?

A

Serosa - it secrets serous fluid to enclose the cavity and reduce friction b/w muscle movements

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6
Q

The ____ ____ ____ contracts to shorten the length of the intestinal segment.

A

longitudinal muscle layer

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7
Q

The ____ ____ ____ contracts to decrease the diameter of the intestinal lumen.

A

Circular muscle layer

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8
Q

What 2 layers work together to propagate gut motility?

A
  1. longitudinal muscle layer
  2. circular muscle layer
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9
Q

Innervation of the GI organs up to the proximal transverse colon are supplied by the ____.

A

Celiac Plexus

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10
Q

Innervation of the descending colon & distal GI tract comes from the ____ ____ ____.

A

Inferior hypogastric plexus

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11
Q

How can the celiac plexus be blocked?

A
  1. transcrural
  2. intraoperative
  3. endoscopic ultrasound-guided
  4. peritoneal lavage
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12
Q

The ____ ____ lies b/w the smooth muscle layers.

What does it do?

A

Myenteric plexus - it regulates the smooth muscle

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13
Q

The submucosal plexus transmits information from the ____ to the ____ & ____.

A

Epithelium
Enteric
Central Nervous Systems

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14
Q

What is the muscalaris mucosa & what does it do?

A

A thin layer of smooth muscle in the mucosa of the GI tract

Functions to move the villi.

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15
Q

What is the lamina propria? What does it contain?

A

The middle layer of the mucosa of the GI tract.

It contains blood vessels & nerve endings.

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16
Q

True or False - there are immune & inflammatory cells in the mucosa of the GI tract.

A

True

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17
Q

What happens in the epithelium of the GI mucosa?

A
  1. where the GI contents are sensed
  2. enzymes are secreted
  3. nutrients are absorbed
  4. waste is excreted
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18
Q

What is the GI tract innervated by?

A

Autonomic nervous system

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19
Q

The extrinsic nervous system has ____ & ____ components.

A

SNS & PNS

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20
Q

The extrinsic SNS is primarily ____ & ____ GI motility

A

inhibitory & decreases

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21
Q

The extrinsic PNS is primarily ____ & ____ GI motility.

A

excitatory & activates

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22
Q

What is the independent nervous system in the GI tract?

What does it control?

A

Enteric Nervous System
Controls motility, secretion, & blood flow

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23
Q

The enteric system is comprised of the ____ ____ & ____ ____.

A

Myenteric Plexus & Submucosal Plexus

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24
Q

What does the myenteric plexus control? How is it carried out?

A

Controls motility

carried out by:
* enteric neurons
* interstitial cells of Cajal (aka ICC cells, GI pacemakers)
* smooth muscle cells

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25
Q

What does the submucosal plexus of the enteric nervous system control?

A

absorption, secretion, & mucosal blood flow

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26
Q

What do the myenteric plexus & submucosal plexus respond to?

A

Sympathetic and parasympathetic stimulation

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27
Q

Anesthesia challenges with upper GI endoscopy

A
  1. sharing airway w/ endoscopist
  2. procedure performed outside of the main OR - don’t have all the bells & whistles
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28
Q

Colonoscopy

A
  • may be diagnostic or therapeutic
  • w/ or w/o anesthesia (rare)
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29
Q

Anesthesia Challenges w/ Colonoscopy

A
  • pt dehydration d/t bowel prep & NPO status
  • renal & CHF pts can be problematic when they are dry
  • MAC (monitored anesthesia care) - BP drops w/ propofol
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30
Q

High Resolution Manometry (HRM)

A
  • pressure catheter measures pressure along the entire esophageal length
  • used to Dx motility disorders
  • anti-reflux procedures
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31
Q

GI series w/ ingested Barium

A
  • radiologic assessment of swallowing function
  • GI transit
  • series of pictures taken under fluoroscopy
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32
Q

Gastric emptying study

A
  • pt fasts for at least 4 hours
  • consumes a meal (eggs) w/ a radiotracer dye in it
  • used to dx gastroparesis/problems emptying the stomach
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33
Q

Small Intestine manometry

A
  • catheter measures contraction pressures & motility of small intestine
  • evaluates contractions during 3 periods:
    (fasting, during a meal, post-prandial)
  • recording time: 4hrs fasting, ingestion of meal, 2hrs post-meal
  • abnormal results grouped into myopathic or neuropathic causes
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34
Q

Lower GI series

A
  • involves the admin of a barium enema
  • barium outlines the intestines & is visible on radiograph
  • allows for detection of colon & rectal abnormalities
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35
Q

Examples of anatomical causes of esophageal disease:

What do they interrupt?

A
  1. diverticula
  2. hiatal hernia
  3. changes associated w/ chronic acid reflux
    * they interrupt the normal pathway of food & change pressure zones of esophagus
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36
Q

Examples of mechanical causes of esophageal disease

A
  1. achalasia
  2. esophageal spasms
  3. Hypertensive LES (lower esophageal sphincter)
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37
Q

Examples of neurological causes of esophageal disease

A
  1. stroke
  2. vagotomy
  3. hormone deficiencies
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38
Q

Most common Sx of Esophageal Disease

A
  1. dysphagia
  2. heartburn
  3. GERD
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39
Q

Dysphagia

A

Difficulty swallowing
2 types

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40
Q

Oropharnygeal dysphagia

A

common after head & neck surgeries

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41
Q

GERD (Gastroesophageal Reflux Disease)

A

Pt experiences effortless return of gastric contents into pharynx
Sxms: heartburn, nausea, “lump in throat”

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42
Q

What is Achalasia?

A
  • one of the most common esophageal diseases
  • neuromuscular disorder of esophagus
  • outflow obstruction d/t inadequate LES tone & dilated hypomobile esophagus
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43
Q

Symptoms of Achalasia:

A
  • dysphagia
  • regurgitation
  • heartburn
  • chest pain
  • hard time getting food to pass adequately
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44
Q

Type 1 Achalasia

A

minimal esophageal pressure
* responds well to myotomy

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45
Q

Type 2 Achalasia:

A

entire esophagus pressurized
* responds well to treatment
* has the best outcomes

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46
Q

Type 3 Achalasia

A

esophageal spasms w/ premature contractions of the esophagus
* has the worst outcomes

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47
Q

Achalasia Tx

A
  • ALL TREATMENTS PALLIATIVE
  • Meds: nitrates, CCBs - relax LES
  • endoscopic botox injections
  • pneumatic dilation - most effective (balloon dilation)
  • Laparascopic Hellar Myotomy - best surgical tx
  • peri-oral endoscopic myotomy (POEM)
  • esophagectomy - only for advanced dx
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48
Q

POEM: peri-oral endoscopic myotomy & risks

A
  • endoscopic division of LES muscle layers
  • 40% develop pneumothorax or pneumoperitoneum
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49
Q

All achalasia pts are ____.

What is indicated b/c of this?

A
  • high risk for aspiration
  • RSI or awake intubation (full stomach)
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50
Q

Diffuse Esophageal Spasms

A
  • spasms that occur in the distal esophagus
  • d/t autonomic dysfunction
  • occur more in elderly
  • Dx: esophagram
  • pain mimics angina
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51
Q

Tx for diffuse esophageal spasms

A

NTG, antidepressants, PDE-I’s

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52
Q

What are Esophageal Diverticula

A

outpouchings in the wall of the esophagus

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53
Q

Pharyngoesophageal Diverticula

A
  • Zenker Diverticulum
  • cause bad breath d/t food retention in the pockets of their throat
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54
Q

Midesophageal Diverticula causes

A
  • deeper down
  • caused by old adhesions, inflamed lymph nodes
55
Q

Epiphrenic Diverticula

A
  • Surpadiaphragmatic
  • pts may experience achalasia
56
Q

All diverticula pts are ____ ____.

What is indicated d/t this?

A

aspiration risks
* removal of particles before putting them to sleep & RSI

57
Q

Hiatal Hernia

A

herniation of the stomach into the thoracic cavity
* occurs through the esophageal hiatus in the diaphragm

58
Q

Cause of hiatal hernia:

A

weakening in anchors of GE junction to the diaphragm

59
Q

Sxms of Hiatal Hernia

A
  • may be asymptomatic
  • often have GERD
60
Q

How does esophageal caner present?

A

Progressive dysphagia & weight loss

61
Q

Why does esophageal cancer have a poor survival rate?

A

Abundant lymphatics in the area leads to lymph node metastasis

62
Q

What are the 2 common types of esophageal cancer?

A
  1. Adenocarcinomas (lower esophagus) - r/t GERD, barrett’s esophagitis, obesity
  2. Squamous cell carcinoma
63
Q

Is an esophagectomy curative or palliative?

A

Can be either

64
Q

How can an esophagectomy be performed?

A
  • transthoracic
  • transhiatal
  • minimally invasive
65
Q

There is a high risk of ____ ____ ____ with esophagectomy surgeries.

A

Recurrent laryngeal nerve injury
* 40% resolve spontaneously

66
Q

Pt concerns r/t esophagectomy

A
  1. pts malnourished pre-op and for months post-op
  2. pancytopenia & dehydration if h/o chemo/radiation
  3. post-esophagectomy pts are high risk of aspiration for life
67
Q

GERD

A

Incompetence of gastro-esophageal junction - leads to reflux
* 15% of adults

68
Q

Sxms of GERD

A
  • heartburn, dysphagia, mucosal injury
69
Q

Reflux contents include ____, ____, ____ ____, & ____.

A
  1. HCl
  2. pepsin
  3. pancreatic enzymes
  4. bile - associated w/ Barret metaplasia & adenocarcinoma
70
Q
A
71
Q

3 mechanisms of GE incompetence

A
  1. Transient LES relaxation - elicited by gastric distention
  2. LES hypotension
  3. Autonomic dysfunction of GE junction
72
Q

What is the normal LES pressure?

GERD pressure?

A
  • measured using manometry
  • LES normal - 29mmHg
  • GERD - 13mmHg
73
Q

Treatment of GERD

A
  1. Avoid trigger foods
  2. Meds: antacids, H2 blockers, PPIs
  3. Surgery
74
Q

What is a Nissen Fundoplication?

A

wrap stomach around esophagus so the stomach muscles tighten where the LES is

75
Q

What is a Toupet?

A

Similar to Nissen - not as high up

76
Q

What is a Linx procedure?

A
  • newer procedure - magnets that open and close around sphincter - less invasive
77
Q

Pre-op Interventions: GERD

A
  1. Cimetidine, Ranitidine - decrease acid production & increase pH
  2. PPIs night before and morning of
  3. sodium citrate - nonparticulate PO antacid (OB c-section)
  4. Metoclopramide - gastrokinetic agent; 3rd line - reserved for DM, obese, pregnant
  5. Aspiration precautions – RSI, cricoid pressure controversial
78
Q
A
79
Q

What is the stomach & what does it do?

A
  • J-shaped sac that serves as a reservoir for large volumes of food
  • mixes & breaks down food to form chyme
  • slows emptying into the small intestine
80
Q

How small must solids be broken down to before entering the duodenum?

A

1-2mm particles

81
Q

How is the motility of the stomach controlled?

A

intrinsic & extrinsic neural regulation

82
Q

SNS stimulation ____ these contractions via the ____ ____.

A

inhibits, sphlanchnic nerve

83
Q

PNS stimulation to the vagus nerve increases the ________________ of the stomach.

A

number & force of contractions

84
Q

The intrinsic nervous system provides ____ for motility.

A

Coordination

85
Q

What is the neurohormonal control of the stomach?

A
  1. Gastrin & Motilin - increase the strength & frequency of contractions
  2. Gastric inhibitory peptide - inhibits contractions
86
Q

What is the most common cause of non-variceal upper GI bleeding?

A

Peptic Ulcer disease
* 10% women, 12% men
* 15,000 deaths/yr

87
Q

PUD may be associated with ____.

A

Helicobacter Pylori

88
Q

Sxms of PUD:

A

burning epigastric pain w/ fasting & improved w/ meals

89
Q

There is a ____ risk of perforation in PUD pts who don’t receive treatment

A

10%

90
Q

PUD Perforation Symptom

A
  1. sudden/severe epigastric pain - acidic secretions leaking into peritoneum (EMERGENCY)
91
Q

What causes moratlity r/t PUD perforation?

A

Shock or perforation >48hrs

92
Q

Gastric Outlet Obstruction onset

A
  • Can be acute or chronic
  • acute d/t edema & inflammation in pyloric channel at the beginning of the duodenum
93
Q

Pyloric obstruction sxms

A

recurrent vomiting, dehydration & hypochloremic alkalosis

94
Q

Tx for gastric outlet obstruction

A
  1. NGT (decompress the stomach)
  2. IV hydration
  3. normally resolves in 72h
95
Q

Type I Gastric Ulcer location

A

Along the lesser curvature close to incisura; no acid hypersecretion

96
Q

Type II Gastric Ulcer

A

2 ulcers - 1st on gastric body, 2nd duodenal
* usually acid hypersecretion

97
Q

Type III Gastric Ulcer

A

Pre-pyloric with acid hypersecretion

98
Q

Type IV Gastric Ulcer

A

At lesser curvature near gastroesophageal junction
* no acid hypersecretion

99
Q

Type V Gastric Ulcer

A

Anywhere in the stomach
* usually seen w/ NSAID use

100
Q

Common causes of gastric ulcers include:

A

NSAIDs, H. Pylori, ETOH

101
Q

Tx for gastric ulcers:

A
  • Antacids, H2 blockers, PPIs
  • Prostaglandin Analogues, cytoprotective agents
102
Q

H. Pylori Tx:

A

Triple Therapy
* 1 Abx
* PPI
* 14 days

103
Q

What is Zollinger Ellison Syndrome?

A

Non B cell islet tumor of the pancreas - causes gastrin hypersecretion
* gastrin stimulates gastric acid secretion
* gastric acid normally inhibits further gastrin release - this is absent in ZE syndrome!

104
Q
A
105
Q

Sxms of Zollinger Ellison Syndrome

A

very high stomach acid levels leading to -
* PUD, erosive esophagitis, diarrhea

106
Q

Incidence of ZE Syndrome

A
  • 0.1-1% of PUD pts
  • males > females
  • ages 30-50
107
Q

Up to 50% of pts w/ gastrinomas are ____ at the time of diagnosis.

A

metastatic

108
Q

Tx of ZE syndrome

A

PPI & Surgical resection of gastrinoma

109
Q

Pts w/ ZE syndrome have: (3 things)

A
  1. increased gastric fluid volume
  2. possible electrolyte imbalances
  3. endocrine abnormalities
110
Q

Pre-op Considerations for ZE Syndrome

A
  • correct electrolytes
  • increase gastric pH w/ meds
  • RSI
111
Q

What does small intestinal motility do? What is the purpose of this?

A

mixes contents of the stomach w/ digestive enzymes
* further reduces particle size & increases solubility

112
Q

What is the major function of the small intestine?

A

circulate the contents & expose them to the mucosal wall
* maximizes the absorption of water, nutrients, & vitamins - before entering large intestine

113
Q

The circular & longitudinal muscle layers coordinate to achieve ____.

A

Segmentation

114
Q

What is segmentation?

A

Isolation of a segment of intestine when 2 nearby areas contract

115
Q

What is the purpose of segmentation?

A

Allows the contents to remain in the intestine long enough for essential substances to be absorbed into circulation

116
Q

What is Segmentation controlled by?

A

Mainly by the enteric nervous system &
modulation of motility by the extrinsic nervous system

117
Q

Reversible causes of small bowel dysmotility:

A
  1. Mechanical Obstruction: hernias, malignancy, adhesions, volvuluses
  2. bacterial overgrowth - alterations in absorptive function
  3. ileus, electrolyte abnormalities, critical illness
118
Q

Structural Irreversible Causes of small bowel dysmotility

A

Scleroderma, connective tissue disorder, IBD

119
Q

Neuropathic Irreversible causes of small bowel dysmotility

A
  1. pseudo obstruction - intrinsic & extrinsic nervous systems are altered
  2. intestines produce weak, uncoordinated contractions
  3. Cannot move food forward - bloating, nausea, vomiting, abd. pain
  4. food stuck in intestines & grows bacteria
120
Q

What is the large intestine?

A

acts as a reservoir for waste & indigestible material before elimination
* it exctracts remaining electrolytes & water

121
Q

Physiology of the large intestine

A
  1. distention of ileum - relaxes ilocecal valve to allow intestinal contents to enter colon
  2. subsequent cecal distention will contract ileocecal valve
  3. colon exhibits giant migrating complexes
122
Q

Giant migrating complexes serve to produce -

how often does this occur?

A

mass movements across the large intestine

6-10x/day

123
Q

Colonic Dysmotility manifests as what 2 symptoms?

A
  1. altered bowel habits
  2. intermittent cramping
124
Q

What are the most common diseases associated with colonic dysmotility?

A

IBS

IBD

125
Q

Rome II criteria for IBS

A

Abdominal discomfort w/ 2 of -
* defecation relieves discomfort
* pain associated w/ abnormal frequency (>3x per day or < 3x/week)
* pain associated w/ a change in the form of the stool

126
Q

In IBD - the contractions & giant migrating complexes are suppressed d/t colonic wall compression by the inflamed mucosa. True or False?

A

False
* the giant migrating complexes remain & are increased in frequency

127
Q

What can the increased frequency of giant migrating complexes in IBD lead to?

A

further compresses the inflamed mucosa
* hemorrhage, thick mucus secretion, significant erosions

128
Q

Repetitive ulceration & scarring may lead to ____ - ____ & ____ ____.

A

Fixed-stenosis & chronic obstruction

129
Q

Factors that increase intra-op Aspiration risk: LONG ASS LIST

A
  1. emergent surgery - full stomach (digestion halted w/ traumas)
  2. full stomach
  3. difficult airway
  4. inadequate anesthesia depth
  5. lithotomy
  6. autonomic neuropathy
  7. Gastoparesis - DM
  8. Pregnancy
  9. Increased intraabdominal pressure
  10. severe illness
  11. morbid obesity
130
Q

Diagnosis for Achalasia

A

esophageal manometry
esophagram

131
Q

What do people w/ achalasia have an increased risk of long-term?

A

esophageal cancer

132
Q

Causes of Achalasia:

A
  1. loss of ganglionic cells of the esophageal myenteric plexus
  2. absence of inhibitory neurotransmitters of the LES
  3. Unopposed cholinergic LES stimulation (LES can’t relax)
  4. Esophageal dilation w/ food unable to pass into stomach
133
Q

Esophageal Dysphagia - 2 types

A

Classified based on physiology
* esophageal dysmotility: sx occur w/ both liquids & solids
* mechanical esophageal dysphagia: sx only occur w/ solid food

134
Q

Upper GI Endoscopy

A
  • May be diagnostic or therapeutic
  • Endoscope placed into esophagus, stomach, pylorus, and duodenum
  • done w/ or w/o anesthesia

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