GI (4) Flashcards

1
Q

The GI tract constitutes approx ____% of total body mass

A

5%

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2
Q

What are the main functions of GI system?

A
  • Motility
  • Digestion
  • Absorption
  • Excretion
  • Circulation
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3
Q

List GI layers from outer most to inner most:

A
  • serosa
  • longitudinal muscle layer
  • circular muscle layer
  • submucosa
  • mucosa
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4
Q

What layers are in the mucosa? (List from outer to inner layer)

A
  • muscularis mucosae
  • lamina propria
  • epithelium
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5
Q

Which muscle layer contracts to shorten the length of the intestinal segment?

A

Longitudinal muscle layer

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6
Q

Which muscle layer contracts to decreases the diameter of the intestinal lumen?

A

Circular muscle layer

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7
Q

Longitudinal and circular muscle layer work together to propagate _______ motility

A

gut

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8
Q

What is the mucosa composed of?

A
  • Muscularis mucosa: function to move the villi
  • Lamina propria: contains blood vessels, nerveendings, and immunecells
  • Epithelium: GI contents are sensed, enzymes are secreted,and nutrients are absorbed
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9
Q

The GI tract is innervated by the _____________ nervous system.

A

Autonomic

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10
Q

What does the GI ANS consist of?

A
  • Extrinsic nervous system
  • Enteric nervous system
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11
Q

What is the function of the extrinsic nervous system?

A
  • PNS and SNS
  • SNS is inhibitory and decreases motility
  • PNS is excitatory and activates motility
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12
Q

What is the function of the enteric nervous system?

A
  • Independent nervous system
  • Controls motility, secretions, and blood flow
  • myenteric plexus and submucosal plexus
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13
Q

What does the celiac plexus innervate?

A

Innervates the proximal GI organs to the transverse colon

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14
Q

Hypogastric plexus innervates:

A

Descending colon and distal GI tract

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15
Q

What approaches can be used to block the celiac plexus?

A
  • Trans-crural
  • Intraoperative
  • Endoscopic ultrasound-guided
  • Peritoneallavage
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16
Q

_________ plexus lies between the smooth muscle layers and regulates the smooth muscle

A

Myenteric

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17
Q

__________ plexus transmits info from the epithelium to the enteric and central nervous systems

A

Submucosal

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18
Q

What is the enteric system composed of?

A
  • Myenteric plexus
  • Submucosal plexus

Both of these plexus respond to SNS and PNS stimulation

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19
Q

What is the function of myenteric plexus?

A

Controls motility→ enteric neuron, interstitial cells of Cajal (aka ICC cells, GI pacemakers), and smooth muscle cells

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20
Q

What is the function of the submucosal plexus?

A
  • absorption
  • secretion
  • mucosal blood flow
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21
Q

What are anesthesia challenges involved with upper endoscopy?

A
  • Sharing airway with endoscopist
  • Usually done without ETT, must closely manage airway
  • Procedure performed outside of the main OR (limited equipment & supplies
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22
Q

What are anesthesia challenges with colonoscopy?

A

Pt dehydration from bowel prep/NPO status

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23
Q

Functions of the stomach:

A
  • Reservoir for food
  • Mixes and breaks fown food to form chyme
  • Empties into the small intestine
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24
Q

What is the purpose of GI barium swallow test?

A

Radiologic assessment of swallow function and GI transit

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25
Q

What is the gastric emptying study?

A

Pt fasts for >4 hours then consumes a meal with a radiotracer (frequent imaging for the next 1-2 hours)

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26
Q

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

A

1-2 mm

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27
Q

What is the motility of the stomach controlled by?

A

Intrinsic and extrinsic neural regulation

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28
Q

What is small intestine manometry?

A
  • Catheter that measures contraction pressures and motility of the small intestine
  • Eval contraction during 3 periods (Fasting, during meal, and post prandial)
  • Abnormal results are grouped into myopathic and neuropathic
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29
Q

PNS stimulates the ____ nerve to increase the number and force of ____:

A

Vagus; contractions

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30
Q

SNS stimulation to the ____ nerve ____ these contractions

A

splanchnic; inhibits

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31
Q

What is a lower GI series for?

A

Barium enema outlines the intestine so its visible on radiograph (allows for detection of colon/rectal abnormalities)

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32
Q

How does neurohormonal control modulate GI movement?

A
  • Gastrin & motilin increase the strength and frequency of contractions
  • Gastric inhibitory peptide inhibits contractions
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33
Q

How are diseases of the esophagus grouped?

A
  • Anatomical
  • Mechanical
  • Neurologic
    Many disease states overlap
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34
Q

What diseases are included in anatomical esophageal diseases?

A
  • Diverticula
  • Hiatal hernia
  • Chronic acid reflux changes
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35
Q

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

A

Peptic ulcer disease

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35
Q

What is the lifetime prevalence of peptic ulcer disease in men and women?

A

10% women
12% men

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36
Q

How many deaths per year occur d/t peptic ulcer disease?

A

15,000

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37
Q

What diseases are included in mechanical esophageal diseases?

A
  • Achalasia
  • Esophageal spasms
  • hypertensive LES
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38
Q

Peptic ulcer disease may be associated with ____ ____

A

Helicobacter pylori

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39
Q

Symptoms of peptic ulcer disease:

A
  • Burning epigastric pain exacerbated with fasting and improved with meals
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40
Q

___% risk of perforation in those who do not receive treatment for peptic ulcer disease

A

10%

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41
Q

What diseases are included in neurologic esophageal diseases?

A
  • Neuro disorders (stroke)
  • Vagotomy
  • Hormone deficiencies
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42
Q

Symptoms of perforation with PUD:

A

Sudden/severe epigastric pain caused by acidic secretions into peritoneum

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43
Q

Mortality in PUD is due to shock or perforation >___

A

> 48 hours

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44
Q

What are the most common S/S of esophageal disease?

A
  • Dysphagia
  • Heartburn
  • GERD
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45
Q

What causes acute gastric outlet obstructions?

A

Acute obstructions caused by edema and inflammation in pyloric channel at the beginning of duodenum
- Onset may be acute or slow

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46
Q

What is dysphagia?

A

Difficulty swallowing (may be oropharyngeal or esophageal)

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47
Q

When is oropharyngeal dysphagia common to occur?

A

After head/neck surgeries

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48
Q

What causes chronic gastric outlet obstruction?

A

Chronic obstructions or stenosis can be caused by repetitive ulceration and scarring

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49
Q

How is esophageal dysphagia classified?

A
  • Esophageal dysmotility: symptoms occur with liquids and solids
  • Mechanical esophageal dysphagia: symptoms only with solid food
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50
Q

What happens with gastroesophageal reflex disease?

A

Effortless return of gastric contents into pharynx
(heartburn, nausea, “lump in throat”)

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51
Q

Treatment for gastric ulcers:

A

H2 blockers, PPIs, prostaglandin analogues, cytoprotective agents

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51
Q

5 types of gastric ulcers are normally caused by what??

A

NSAIDs, H. Pylori, ETOH

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52
Q

Neuromuscular disorder of the esophagus creating an outflow obstruction d/t inadequate LES tone and a dilated hypomobile esophagus:

A

Achalasia

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53
Q

Treatment for H. Pylori gastric ulcers:

A

Triple therapy - (2 abx +PPI) x 14 days

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54
Q

What causes achalasia?

A
  • loss of ganglionic cells of the esophageal myenteric plexus
  • absence of LES inhibitory neurotransmitters
  • LES cant relax (unopposed cholinergic stimulation)
  • Esophageal dilation with food unable to move forward
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55
Q

5 types of gastric ulcers:

A
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56
Q

What is Zollinger Ellison syndrome?

A

Non B cell pancreatic tumor (gastrinoma) that causes hypersecretion of gastrin

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57
Q

What are S/S of esophageal disease?

A
  • dysphagia
  • regurgitation
  • heartburn
  • chest pain
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58
Q

What is absent in zollinger ellison syndrome?

A

The negative feedback look where gastrin stimulates gastric acid secretion, and gastric acid normally inhibits further gastrin release

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59
Q

What is long term achalasia associated with?

A

Increased risk of esophageal cancer

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60
Q

How is Achalasia diagnosed?

A

Esophageal manometry and/or esophagram

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61
Q

Symptoms of zollinger ellison syndrome:

A
  • Peptic ulcer disease
  • Erosive esophagitis
  • Diarrhea
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62
Q

What are the 3 classes of achalasia?

A
  • Type 1: minimal esophageal pressure, responds well to myotomy
  • Type 2: entire esophagus pressurized; responds well to treatment, has best outcomes
  • Type 3: esophageal spasms w/premature contractions; has worst outcomes
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63
Q

Prevalence of zollinger ellison syndrome:

A
  • Occurs in 0.1-1% of PUD patients
  • M>F
  • most commonly between ages 30-50
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64
Q

What are treatment options for achalasia?

A

All treatments are palliative
- Meds: nitrates/CCB to relax LES
- Endoscopic botox injections
- Pneumatic dilation
- Laparoscopic hellar myotomy
- peri-oral endoscopic myotomy (PEOM)
- Esophagectomy

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65
Q

Up to ___% of patients with ____ are metastatic at time of diagnosis

A

50%; gastrinomas

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66
Q

What is the most effective non-surgical treatment for achalasia?

A

Pneumatic Dilation

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67
Q

What is the best surgical treatment for achalasia treatment?

A

Laparoscopic Hellar myotomy

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68
Q

Treatment for ZES:

A
  • PPIs
  • Surgical resection of gastrinoma
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69
Q

Considerations for patients with ZES:

A
  • Increased gastric volume (RSI these patients)
  • Electrolyte imbalances
  • Endocrine abnormalities
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70
Q

Preop considerations for ZES:

A
  • Correct electrolytes
  • increase gastric pH with meds
  • RSI
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71
Q

Functions of the small intestine:

A
  • Motility mixes the nutrients with digestive enzymes, further reducing particle size and increasing solubility
  • Major function is to circulate contents and expose them to the mucosal wall to maximize absorption
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72
Q

What are anesthesia considerations for patients with Achalasia?

A
  • increase risk for aspiration
  • RSI or awake intubation indicated
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73
Q

Where do most esophageal spasms occur? What causes them?

A

Spasms that usually occur in distal esophagus likely from autonomic dysfunction

74
Q

Esophageal spasms are more common in __________

75
Q

How are esophageal spasms diagnosed?

A

Esophagram

76
Q

In the small intestine, the ____ and ____ muscle layers coordinate to achieve ____

A

Circular and longitudinal; achieve segmentation

77
Q

Pain from esophageal spasm mimics_______

78
Q

What are treatments for esophageal spasms?

A
  • Nitro
  • antidepressants
  • phosphodiesterase inhibs
79
Q

What is esophageal diverticula?

A
  • Outpouchings in the wall of the esophagus
  • Increases risk for aspiration: need to remove particles and RSI
80
Q

What are different types of esophageal diverticula?

A
  • Pharyngoesophageal (Zenker diverticulum): bad breath d/t food retention
  • Midesophageal: may be caused by old adhesions or inflamed lymph nodes
  • Epiphrenic (supradiaphragmatic): pts may experience achalasia
81
Q

What is segmentation in the small intestine?

A

Occurs when two nearby areas contract and isolate a segment to hold the contents in place long enough to be absorbed into the circulation

82
Q

What is segmentation in the small intestine controlled by?
What about motility?

A

The enteric nervous system with motility controlled by the extrinsic nervous system

83
Q

What is a hiatal hernia?

A
  • Herniation of stomach into thoracic cavity, occurs through the esophageal hiatus in the diaphragm
  • Weakening in connective tissues that anchor the GE junction to the diaphragm
  • May be asymptomatic often have GERD
84
Q

Reversible causes of small bowel dysmotility:

A
  • mechanical obstruction such as hernias, malignancy, adhesions, volvuluses
  • bacterial overgrowth leading to alterations in absorptive function
  • ileus, electrolyte abnormalities and critical illness
85
Q

________: 100,000 people in the US Have esophageal cancer

86
Q

How does esophageal cancer present?

A

Progressive dysphagia and weight loss

87
Q

Nonreversible causes of small bowel dysmotility can be classified as what two types?

A

Structural or neuropathic

88
Q

Why is esophageal cancer survival rate poor? Where are most of these cancers located?

A
  • Abundant lymphatics leads to lymph node metastasis
  • Most are adenocarcinomas in the lower esophagus (related to GERD, Barretts, obesity)
89
Q

What are structural causes of small bowel dysmotility?

A
  • Scleroderma
  • Connective tissue disorders
  • IBD
90
Q

What are the 2 different types of esophageal cancers?

A
  • Adenocarcinomas (Most common)
  • Squamous cell carcinoma
91
Q

What can be done for esophageal cancer to cure or palliative care?

A

Transthoracic, transhiatal, or minimally invasive Esophagectomy

92
Q

What is high risk associated with esophagectomy?

A

Recurrent laryngeal nerve injury (40% resolve spontaneously)

93
Q

Post esophagectomy patients are high risk for ___________ for life

A

aspiration

94
Q

What are neuropathic causes of small bowel dysmotility?

A

Pseudo-obstruction caused by intrinsic and extrinsic nervous system dysfunction
- only produce weak, uncoordinated contractions
- leads to bloating, nausea, vomiting, abdominal pain

95
Q

What causes GERD?

A

Incompetence of the gastro-esophageal junction, leading to reflux

96
Q

What are S/S of GERD? What percent of adults have GERD?

A
  • Heartburn
  • Dysphagia
  • Mucosal injury

15% of adults

97
Q

What does GERD reflux contents include?

A
  • HCl
  • Pepsin
  • Pacreatic enzymes
  • Bile
98
Q

Functions of the large intestine:

A
  • Reservoir for waste and indigestible material before elimination
  • extracts remaining electrolytes and water
99
Q

Bile reflux is associated with ___________ __________ and adenocarcinoma

A

Barrett metaplasia

100
Q

The colon also exhibits giant ____ ____

A

migrating complexes

101
Q

What 3 mechanisms cause gastro-esophageal incompetence?

A
  • Transient LES relaxation from gastric distention
  • LES hypotension
  • Autonomic dysfunction of GE junction
102
Q

What are giant migrating complexes for in the large intestine?

How often do they occur?

A

Serve to produce mass movements across the large intestine

In a healthy state, they occur approx. 6-10x/day

103
Q

What are the two primary symptoms of colonic dysmotility?

A
  • altered bowel habits
  • intermittent cramping
104
Q

What is normal LES pressure? What is LES pressure with GERD?

A

Norm: 29mmHg
GERD: 13mmHg

105
Q

Treatments for GERD:

A
  • Avoidance of trigger foods
  • Meds: Antacids, H2 blockers, PPIs
  • Surgery: Nissen Fundoplication, Toupet, LINX
106
Q

What are some preop interventions for patients with GERD?

A
  • Cimetidine, Ranitidine-↓acid secretion & ↑ gastric pH
  • PPI’s generally given night before and morning of
  • Sodium Citrate- PO nonparticulate antacid
  • Metoclopramide
  • Aspiration precautions (RSI)
107
Q

What are the most common diseases associated with colonic dysmotility?

A

IBS and IBD

108
Q

What can happen if you have increased frequency of giant migrating complexes?

A

Further compresses the inflamed mucosa, which can lead to significant erosions and hemorrhage

109
Q

Which patients usually get reglan in preop?

A
  • Diabetics (gastroparesis)
  • Obese
  • Pregnant

reglan= gastrokinetic

110
Q

In IBD, contractions are suppressed due to ____, but the giant migrating complexes ____

A

inflammation; remain

111
Q

What is the 2nd most common inflammatory disorder after RA?

A

Inflammatory bowel disease

112
Q

What is the incidence of IBD?

A

18:100,000 people

113
Q

What are factors that increase intraop aspiration risk?

A
  • Emergent surgery
  • Full Stomach
  • Difficult airway
  • Inadequate anesthesia depth
  • Lithotomy
  • Autonomic Neuropathy
  • Gastroparesis
  • DM
  • Pregnancy
  • ↑ Intraabdominal pressure
  • Severe Illness
  • Morbid Obesity
114
Q

What is ulcerative colitis?

A

Mucosal disease of part or all of the colon

115
Q

What can occur in severe cases of ulcerative colitis?

A

The mucosa can be hemorrhagic, edematous and ulcerated

116
Q

Symptoms of IBD:

A
  • Diarrhea
  • Rectal bleeding
  • Crampy abdominal pain
  • N/V
  • Fever
  • Weight loss
117
Q

Lab values for IBD:

A

-↑plts
-↑erythrocyte sedimentation rate
- decreased H&H
- decreased albumin

118
Q

What warrants surgical colectomy?

A

Hemorrhage requiring 6+ units of blood in 24-48 hours

119
Q

What triggers toxic megacolon?

A

Electrolyte disturbances

120
Q

How many cases of toxic megacolon resolve?

A

about 1/2 resolve and 1/2 require colectomy

121
Q

Mortality rate of colon perforation:

122
Q

What part of the bowel does Crohn’s disease affect?

A

Acute or chronic inflammatory process that may affect any/all of the bowel

123
Q

What is the most common site for Crohn’s and how does it present?

A

Terminal ileum; presents with ileocolitis, RLQ and diarrhea

124
Q

Symptoms for Crohn’s disease:

A
  • Weight loss
  • Fear of eating
  • Anorexia
  • Diarrhea
125
Q

In Crohn’s, persistent inflammation gradually progresses to what?

A

Fibrous narrowing and stricture formation

126
Q

In Crohn’s extensive inflammation leads to what?

A

Loss of absorptive surfaces, resulting in malabsorption

127
Q

1/3 of Crohn’s patients have additional symptoms of what?

A
  • Arthritis
  • Dermatitis
  • Kidney stones
128
Q

In Crohn’s, diarrhea decreases and is replaced by what?

A

Chronic bowel obstruction

129
Q

Medical treatment for IBD:

A
  • 5-acetylsalicyclic acid (mainstay for IBD)
  • PO/IV glucocorticoids during flares
  • Antibiotics: Rifaximin, flagyl, cipro
  • Purine analogues
130
Q

Surgery considerations for IBD treatment:

A
  • Last resort - resected segment should be as conservative as possible
  • small intestine resection should be limited to <1/2 length
    >2/3 resection leads to “short bowel syndrome” - requiring TPN
131
Q

Where do 95% of carcinoid tumors originate from?

A

GI tract
(but may occur in any area of GI tissue)

132
Q

What do carcinoid tumors secrete?

A

Peptides and vasoactive substances
- Gastrin, insulin, somatostatin, motilin, neurotensin, tachykinins, glucagon, serotonin, other biological actives

133
Q

Carcinoid syndroms occurs in ___ of patients with carcinoid tumors

134
Q

Symptoms of carcinoid tumors:

A
  • Flushing
  • Diarrhea
  • HTN/HoTN
  • Bronchoconstriction
  • May acquire right heard endocardial fibrosis
  • Left heart generally more protected as the lungs clear some of the vasoactive substances
135
Q

What is carcinoid syndrome?

A

When large amounts of serotonin and vasoactive substances reach systemic circulation

136
Q

Diagnosis of carcinoid syndrome:

A
  • Urinary or plasma serotonin levels
  • CT/MRI
137
Q

Treatment for carcinoid syndrome:

A
  • Avoid serotonin-triggers
  • Serotonin antagonists
  • Somatostatin analogues
138
Q

Preop considerations for carcinoid syndrome:

A

Octreotide before surgery and prior to tumor manipulation to attenuate volatile hemodynamic changes

139
Q

Incidence of acute pancreatitis:

A

Incidence has increased 10 fold since 1960s
- likely due to↑alcoholism along with better diagnostics

140
Q

Pancreas contains numerous ____:

A

Digestive enzymes

141
Q

What is autodigestion normally prevented by?

A
  • Proteases packaged in precursor form
  • Proteases inhibitors
  • Low intra-pancreatic calcium, which decreases trypsin activity
    *failure of any of these mechanisms can trigger pancreatitis
142
Q

What are the most common causes of acute pancreatitis?

A

Gallstones and alcohol abuse (60-80%)

143
Q

How do gallstones cause acute pancreatitis?

A

Obstruct ampulla of vater, causing pancreatic ductal HTN

144
Q

Pancreatitis is also seen in what patients?

A
  • Immunodeficiency syndrome
  • Hyperparathyroidism
    -↑Ca++
145
Q

Symptoms of acute pancreatitis:

A
  • Excruciating epigastric pain that radiates to back
  • N/V
  • abdominal distention
  • steatorrhea
  • ileus
  • fever
  • tachycardia
  • HoTN
146
Q

Hallmark labs of acute pancreatitis:

A

Increased serum amylase and lipase

147
Q

Imaging for acute pancreatitis:

A
  • Contrast CT or MRI,
  • endoscopic US
148
Q

What are the complications of acute pancreatitis?

A

25% experience serious complications such as shock, ARDS, renal failure, necrotic pancreatic abscess

149
Q

Treatment for acute pancreatitis:

A
  • Aggressive IVF
  • NPO to rest pancreas
  • Enteral feeding (over TPN)
  • Opioids
150
Q

Why is enteral feeding preferred over TPN in patients with acute pancreatitis?

A

TPN is associated with greater risk of infectious complications

151
Q

What is the purpose of an ERCP with acute pancreatitis?

A
  • Fluoroscopic examination of biliary and pancreatic ducts
  • Interventions include stone removal, stent placement, sphincterotomy, hemostasis
152
Q

Is upper or lower GI bleeding more common?

153
Q

In upper GI bleeds, ___% of blood loss will lead to HoTN and tachycardia

154
Q

Orthostatic HoTN normally indicates HCT ____?

155
Q

What does melena indicate?

A

bleed is above the cecum (where SI meets colon)

156
Q

What are BUN values for upper GI bleeding and why?

A

> 40 mg/dL due to absorbed nitrogen into bloodstream

157
Q

What is the diagnostic procedure of choice for upper GI bleeding?

A

EGD
- endoscopic ulcer ligation
- ligation of bleeding varices

158
Q

What is the last resort for uncontrolled variceal bleeding?

A

Mechanical balloon tamponade

159
Q

Causes of lower GI bleeding:

A
  • Diverticulosis
  • Tumors
  • Colitis
160
Q

For lower GI bleeds, what can be performed when hemodynamically stable?

A

Unprepped sigmoidoscopy

161
Q

What does persistent lower GI bleeding warrant?

A

Angiography and embolic therapy

162
Q

What is an ileus?

A
  • Characterized by massive dilation of the colon without mechanical obstruction
  • loss of peristalsis leads to distention of the colon
163
Q

What can cause an ileus?

A
  • Electrolyte disorders
  • Immobility
  • Excessive narcotics
  • Anticholinergics
164
Q

Ileus are also thought to be due to what imbalance?

A

Neural-input imbalance of excessive SNS stimulation along with inadequate PNS input to the colon

165
Q

Treatment for ileus:

A
  • Restore electrolyte imbalance
  • Hydrate
  • Mobilize
  • NG suction
  • Enemas
166
Q

What medication can produce immediate results in 80-90% of ileus?

A

Neostigmine 2-2.5 mg over 5 minutes
*cardiac monitoring required

167
Q

If an ileus is left untreated, what may happen?

A

Ischemia and perforation

168
Q

In preop, patients are often nervous and ____ charged:

A

Sympathetically

169
Q

What happens to the GI system when you’re anxious in preop?

A

Inhibition of GI activity is directly proportional to the amount of norepinephrine secreted from SNS stimulation
*higher anxiety = higher GI inhibition

170
Q

What do volatile anesthetics depress in the GI system?

A

Electrical, contractile and propulsive GI activity

171
Q

What is the first part of the GI tract to recover?

A

The small intestine

172
Q

When does the stomach and colon recover postop?

A

Stomach = 24 hours
Colon = 30-40 hours

173
Q

Volatile agents coupled with what can inhibit GI function and motility?

A

SNS hyperactivity associated with surgery

174
Q

Nitrous oxide is __x more soluble than ___ in the blood and will diffuse into gas containing cavities

A

30x more soluble than nitrogen - will diffuse out of the blood faster than nitrogen

175
Q

When giving nitrous, GI distention correlates with what?

A

The pre-existing amount of gas in the bowel, as well as the duration and concentration of nitrous administered

176
Q

When should nitrous be avoided?

A

Lengthy abdominal surgeries or when the bowel is already distended

177
Q

Do NMBDs affect GI motility?

A

NO - only skeletal muscle, so the GI motility remains intact

178
Q

How does neostigmine increase bowel peristalsis?

A

Increasing frequency and intensity of contractions

179
Q

Why is an anticholinergic often given with neostigmine?

A

To counteract the bradycardia associated with neostigmine

180
Q

Does sugammadex affect GI motility?

181
Q

Opioids are known to cause what??

A

reduced GI motility and constipation

182
Q

What receptors do opioids stimulate?

A

Mu, Delta, Kappa

183
Q

Where is there a high density of peripheral mu-opioid receptors?

A

Myenteric and submucosal plexuses

184
Q

What is caused by activation of mu-receptors?

A

Delayed gastric emptying and slower GI transit

185
Q

What are some other adverse effects of anesthesia on the GI system?

A
  • Nausea
  • Anorexia
  • Delayed digestion
  • Abdominal pain
  • Constipation