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Assessment '24 - Mordecai > T4 - GI Assessment > Flashcards

T4 - GI Assessment Flashcards

1
Q

What percentage of the total human body mass does the GI tract constitute?

A

Approximately 5%.

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2
Q

What are the main functions of the GI tract?

A

Motility, digestion, absorption, excretion, and circulation.

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3
Q

What are the layers of the GI tract from outermost to innermost?

A

Serosa, longitudinal muscle layer, circular muscle layer, submucosa, and mucosa.

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4
Q

What are the components within the mucosa from outermost to innermost?

A

Muscularis mucosae, lamina propria, and epithelium.

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5
Q

What is the function of the serosa?

A

secrete serous fluid to enclose the cavity and reduce friction between muscle movements.

It is a smooth membrane of thin connective tissue and cells

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6
Q

What is the function of the longitudinal muscle layer in the GI tract?

A

It contracts to shorten the length of the intestinal segment.

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7
Q

What does the circular muscle layer do?

A

It contracts to decrease the diameter of the intestinal lumen.

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8
Q

How do the longitudinal and circular muscle layers work together?

A

They work together to propagate gut motility.

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9
Q

Which plexus supplies innervation to the GI organs up to the proximal transverse colon?

A

The celiac plexus.

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10
Q

Where does the innervation of the descending colon and distal GI tract come from?

A

The inferior hypogastric plexus.

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11
Q

What are some of the approaches to block the celiac plexus?

A
  • Transcrural
  • Intraoperative
  • Endoscopic ultrasound-guided
  • Peritoneal lavage
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12
Q

Where is the myenteric plexus located and what is its function?

A

between the smooth muscle layers

regulates their function.

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13
Q

What is the role of the submucosal plexus in the GI tract?

A

transmits information from the epithelium to the enteric and central nervous systems.

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14
Q

What is the muscularis mucosa and what is its function?

A

It is a thin layer of smooth muscle that moves the villi in the GI tract.

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15
Q

What is the lamina propria and what does it contain?

A

The lamina propria contains blood vessels, nerve endings, and immune and inflammatory cells.

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16
Q

What are the functions of the epithelium in the GI tract?

A

The epithelium is involved in sensing the GI contents, secreting enzymes, absorbing nutrients, and excreting waste.

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17
Q

What are the components of the GI tract’s autonomic nervous system (ANS)?

A

The GI ANS consists of the extrinsic nervous system with sympathetic (SNS) and parasympathetic (PNS) components, and the enteric nervous system.

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18
Q

What is the primary function of the extrinsic SNS in the GI tract?

A

It is primarily inhibitory and decreases GI motility.

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19
Q

How does the extrinsic PNS affect the GI tract?

A

It is primarily excitatory and activates GI motility.

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20
Q

What does the enteric nervous system control?

A

motility

Absorption/secretion

blood flow

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21
Q

What is the enteric system comprised of what plexuses?

A

The myenteric plexus and submucosal plexus.

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22
Q

What does the myenteric plexus control and what are its components?

A

motility

enteric neurons,
interstitial cells of Cajal (ICC cells or GI pacemakers)
smooth muscle cells.

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23
Q

What functions are regulated by the submucosal plexus?

A

Absorption, secretion, and mucosal blood flow.

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24
Q

How do the myenteric and submucosal plexuses respond to stimulation?

A

They respond to both sympathetic and parasympathetic stimulation.

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25
Q

What can an Upper Gastrointestinal Endoscopy be used for?

A

Diagnostic or therapeutic purposes

Endoscope can be placed into the esophagus, stomach, pylorus, and duodenum.

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26
Q

Can Upper Gastrointestinal Endoscopy be done with anesthesia?

A

Yes, it may be done with or without anesthesia.

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27
Q

What are some anesthesia challenges during an Upper Gastrointestinal Endoscopy?

A

Sharing the airway with the endoscopist and performing the procedure outside of the main OR.

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28
Q

What can a Colonoscopy be used for?

A

It may be diagnostic or therapeutic/interventional.

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29
Q

What are some anesthesia challenges during a Colonoscopy?

A

Patient dehydration due to bowel preparation and NPO (nil per os, nothing by mouth) status.

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30
Q

What does High Resolution Manometry (HRM) measure?

A

HRM measures pressures along the entire length of the esophagus.

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31
Q

What is HRM generally used to diagnose?

A

Motility disorders of the esophagus.

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32
Q

What is a GI series with ingested barium used for?

A

It is a radiologic assessment of swallowing function and GI transit.

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33
Q

How is a gastric emptying study conducted?

A

The patient fasts for at least 4 hours, then consumes a meal with a radiotracer, followed by continuous or frequent imaging for the next 1-2 hours.

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34
Q

What does small intestine manometry measure?

A

It measures contraction pressures and motility of the small intestine.

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35
Q

How are contractions evaluated during small intestine manometry?

A

They are evaluated during three periods: fasting, during a meal, and post-prandial, typically with 4 hours of fasting, then a meal, followed by 2 hours post-meal recording.

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36
Q

What can abnormal results from small intestine manometry indicate?

A

Abnormal results can be grouped into myopathic and/or neuropathic causes.

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37
Q

What does a lower GI series involve and what does it detect?

A

administration of a barium enema to outline the intestines on radiographs

detection of colon and rectal anatomical abnormalities.

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38
Q

Into what categories are diseases of the esophagus grouped?

A

Anatomical
Mechanical
Neurologic
Although many disease states overlap

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39
Q

What are some anatomical causes of esophageal diseases?

A

Diverticula,
hiatal hernia
changes associated with chronic acid reflux

can interrupt the normal pathway of food and change the pressure zones of the esophagus.

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40
Q

What are mechanical causes of esophageal diseases?

A

Achalasia (failure of smooth muscle fibers to relax)

esophageal spasms

hypertensive lower esophageal sphincter (LES)

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41
Q

What can neurologic causes of esophageal diseases be a result of?

A

stroke

vagotomy

hormone deficiencies

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42
Q

What are the most common symptoms of esophageal disease?

A

Dysphagia

heartburn

GERD

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43
Q

What is dysphagia and how is it classified?

A

Dysphagia is difficulty swallowing

oropharyngeal

esophageal

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44
Q

What is a common cause of oropharyngeal dysphagia?

A

It’s commonly seen after head and neck surgeries.

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45
Q

How can esophageal dysphagia be categorized based on physiology?

A
  • Esophageal dysmotility: Symptoms occur with both liquids and solids.
  • Mechanical esophageal dysphasia: Symptoms only occur with solid food.
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46
Q

What is GERD and what are its common symptoms?

A

GERD is the effortless return of gastric contents into the pharynx, often causing heartburn, nausea, and a sensation of a “lump in the throat.”

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47
Q

What is achalasia?

A

Achalasia is a neuromuscular disorder of the esophagus characterized by inadequate LES tone leading to outflow obstruction, and a dilated, hypomobile esophagus.

NCBI: Achalasia is an esophageal smooth muscle motility disorder that occurs due to a failure of relaxation of the lower esophageal sphincter. This condition causes a functional obstruction at the gastroesophageal junction.

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48
Q

What causes achalasia?

A

loss of ganglionic cells in the esophageal myenteric plexus,

absence of inhibitory neurotransmitters of the LES

unopposed cholinergic LES stimulation preventing relaxation.

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49
Q

What are the symptoms of achalasia?

A

Dysphagia, regurgitation, heartburn, and chest pain.

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50
Q

How is achalasia diagnosed?

A

With esophageal manometry and/or esophagram.

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51
Q

What are the three classes of achalasia and how do they respond to treatment?

A
  • Type 1: Minimal esophageal pressure, responds well to myotomy.
  • Type 2: Entire esophagus pressurized; responds well to treatment and has the best outcomes.
  • Type 3: Esophageal spasms with premature contractions; has the worst outcomes.
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52
Q

What is the goal of achalasia treatments?

A

All treatments for achalasia are palliative, aiming to alleviate symptoms.

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53
Q

What medications are used for achalasia treatment?

A

Nitrates

calcium channel blockers (CCBs)

to relax the lower esophageal sphincter (LES).

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54
Q

What endoscopic treatment is used for achalasia?

A

Endoscopic botox injections

to temporarily relax the LES.

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55
Q

Which non-surgical treatment is most effective for achalasia?

A

Pneumatic dilation.

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56
Q

What is considered the best surgical treatment for achalasia?

A

Laparoscopic Heller Myotomy.

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57
Q

What is a Peri-oral Endoscopic Myotomy (POEM) and its risks?

A

POEM is an endoscopic division of LES muscle layers with a 40% risk of developing pneumothorax or pneumoperitoneum.

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58
Q

When is esophagectomy considered for achalasia?

A

Only in the most advanced disease states.

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59
Q

What is the anesthesia consideration for patients with achalasia?

A

Patients are at increased risk for aspiration; Rapid Sequence Induction (RSI) or awake intubation is indicated.

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60
Q

What are Diffuse Esophageal Spasms and where do they commonly occur?

A

Spasms that usually occur in the distal esophagus and are likely due to autonomic dysfunction.

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61
Q

Who is more commonly affected by Diffuse Esophageal Spasms?

A

More common in the elderly.

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62
Q

How is Diffuse Esophageal Spasm diagnosed?

A

Diagnosed on an esophagram.

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63
Q

What can the pain from Diffuse Esophageal Spasms mimic?

A

Pain can mimic angina.

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64
Q

What are some treatments for Diffuse Esophageal Spasms?

A

Treatments include nitroglycerin (NTG), antidepressants, and phosphodiesterase inhibitors (PD-Is).

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65
Q

What are Esophageal Diverticula?

A

Outpouchings in the wall of the esophagus.

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66
Q

What is Pharyngoesophageal (Zenker) Diverticulum and a symptom associated with it?

A

A type of esophageal diverticulum associated with bad breath due to food retention.

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67
Q

What might cause Midesophageal Diverticula?

A

May be caused by old adhesions or inflamed lymph nodes.

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68
Q

What condition may patients with Epiphrenic (supradiaphragmatic) Diverticula also experience?

A

Patients may also experience achalasia.

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69
Q

What are the aspiration risks associated with Esophageal Diverticula, and what is indicated for these patients?

A

All types of esophageal diverticula pose an aspiration risk. Removal of particles and Rapid Sequence Induction (RSI) are indicated.

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70
Q

What is a Hiatal Hernia?

A

A herniation of the stomach into the thoracic cavity through the esophageal hiatus in the diaphragm.

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71
Q

What can cause a Hiatal Hernia?

A

It can be caused by weakening in the anchors of the gastroesophageal (GE) junction to the diaphragm.

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72
Q

What are common symptoms associated with a Hiatal Hernia?

A

It may be asymptomatic but is often associated with GERD (Gastroesophageal Reflux Disease).

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73
Q

What is the prevalence of Esophageal Cancer in the US?

A

4-5 per 100,000 people in the US.

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74
Q

How does esophageal cancer typically present?

A

With progressive dysphagia and weight loss.

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75
Q

Why is the survival rate poor for esophageal cancer?

A

Because the abundant lymphatics lead to lymph node metastasis.

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76
Q

What is the most common type of esophageal cancer and its risk factors?

A

adenocarcinomas in the lower esophagus

related to GERD, Barrett’s esophagus, and obesity.

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77
Q

What other type of cancer accounts for esophageal cancers?

A

Squamous cell carcinoma.

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78
Q

What is the purpose of an esophagectomy in the context of esophageal cancer?

A

curative or palliative reasons.

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79
Q

How can an esophagectomy be performed?

A

It may be performed transthoracically, transhiatally, or using minimally invasive techniques.

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80
Q

What is a common complication of esophagectomy and its prognosis?

A

High risk of recurrent laryngeal nerve injury, with about 40% resolving spontaneously.

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81
Q

What nutritional status is common in patients preoperatively and post-esophagectomy?

A

Patients often present malnourished before the operation and may remain so for many months after.

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82
Q

What complications may present if there is a history of chemotherapy or radiation prior to esophagectomy?

A

Pancytopenia and dehydration.

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83
Q

What is a long-term risk for patients after esophagectomy?

A

They are at a very high risk for aspiration for life.

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84
Q

What causes GERD?

A

Incompetence of the gastroesophageal junction, leading to reflux.

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85
Q

What are common symptoms of GERD?

A

Heartburn, dysphagia, and mucosal injury.

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86
Q

Prevalence of GERD in adults?

A

Occurs in 15% of adults.

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87
Q

What does reflux content include in GERD?

A

Hydrochloric acid (HCl), pepsin, pancreatic enzymes, and bile.

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88
Q

How is bile reflux associated with Barrett metaplasia and adenocarcinoma?

A

Bile reflux is associated with Barrett metaplasia and an increased risk of adenocarcinoma.

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89
Q

What are the three mechanisms of gastroesophageal incompetence in GERD?

A
  • Transient lower esophageal sphincter (LES) relaxation, elicited by gastric distention.
  • LES hypotension (normal LES pressure is 29 mmHg; average GERD pressure is 13 mmHg).
  • Autonomic dysfunction of the GE junction.
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90
Q

What lifestyle intervention is recommended for GERD treatment?

A

Avoidance of trigger foods.

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91
Q

What medications are commonly used for GERD?

A

Antacids, H2 blockers, and Proton Pump Inhibitors (PPIs).

92
Q

What are some surgical options for GERD?

A

Nissen Fundoplication, Toupet fundoplication, and LINX device placement.

93
Q

What preoperative interventions are used for GERD patients?

A
  • Cimetidine and Ranitidine (H2-Blockers) to decrease acid secretion and increase pH.
  • PPIs generally given the night before and the morning of surgery.
  • Sodium Citrate, an oral nonparticulate antacid.
94
Q

What medication can be given to enhance gastric emptying?

A

Metoclopramide, which is a gastrokinetic; often reserved for diabetics, obese, and pregnant patients.

95
Q

What are aspiration precautions for patients with GERD?

A

Aspiration precautions include RSI (Rapid Sequence Induction). Cricoid pressure is controversial.

96
Q

Factors that increase intra-op aspiration risk:

A
  • Emergent surgery
  • Full Stomach
  • Difficult airway
  • Inadequate anesthesia depth
  • Lithotomy
  • Autonomic Neuropathy
  • Gastroparesis
  • DM
  • Pregnancy
  • ↑ Intraabdominal pressure
  • Severe Illness
  • Morbid Obesity
97
Q

Pre-op Asessment - Aspiration risk video:

A

https://www.youtube.com/watch?v=E8XD8iv7BaM

98
Q

What are the functions of the stomach?

A

It serves as a reservoir for large volumes of food, mixes and breaks down food to form chyme, and controls emptying into the small intestine.

99
Q

What size must solids be broken down into before entering the duodenum?

A

Solids must be broken down into 1-2 mm particles.

100
Q

What regulates the motility of the stomach?

A

Motility is controlled by both intrinsic and extrinsic neural regulation.

101
Q

How does parasympathetic stimulation affect stomach contractions?

A

It increases the number and force of contractions via the vagus nerve.

102
Q

What is the effect of sympathetic stimulation on stomach contractions?

A

It inhibits these contractions via the splanchnic nerve.

103
Q

What provides coordination for stomach motility?

A

The intrinsic nervous system.

104
Q

Which substances are involved in neurohormonal control of stomach motility and how do they affect it?

A
  • Gastrin and motilin increase the strength and frequency of contractions.
  • Gastric inhibitory peptide inhibits contractions.
105
Q

What is the lifetime prevalence of Peptic Ulcer Disease?

A

10% in women and 12% in men.

106
Q

How many deaths per year are attributed to Peptic Ulcer Disease?

A

15,000 deaths per year.

107
Q

What is often associated with Peptic Ulcer Disease?

A

Helicobacter pylori infection.

108
Q

What are common symptoms of Peptic Ulcer Disease?

A

Burning epigastric pain that is exacerbated with fasting and improved with meals.

109
Q

What is the risk of perforation in Peptic Ulcer Disease without treatment?

A

There is a 10% risk of perforation.

110
Q

What are the signs of a perforated peptic ulcer?

A

Sudden and severe epigastric pain due to acidic secretions entering the peritoneum.

111
Q

What are common causes of mortality in Peptic Ulcer Disease?

A

Mortality is due to shock or perforation if untreated for more than 48 hours.

112
Q

What is gastric outlet obstruction?

A

Gastric outlet obstruction is a blockage that prevents food from leaving the stomach and entering the small intestine.

113
Q

What are potential causes of gastric outlet obstruction?

A

Causes can include peptic ulcers, malignancies, gastric polyps, or strictures following inflammation.

114
Q

What are common symptoms of gastric outlet obstruction?

A

Symptoms often include vomiting, abdominal pain, bloating, and a reduced appetite.

115
Q

How is gastric outlet obstruction diagnosed?

A

It can be diagnosed using imaging studies like an upper gastrointestinal series or endoscopy.

116
Q

What treatments are available for gastric outlet obstruction?

A

Treatments may involve endoscopic procedures to remove the obstruction, surgical intervention, or medications to reduce inflammation and promote healing.

117
Q

How many types of gastric ulcers are there?

A

There are five types of gastric ulcers.

118
Q

What are common causes of gastric ulcers?

A

NSAIDs,

infection with H. pylori

alcohol consumption (ETOH)

119
Q

What are the treatments for gastric ulcers?

A

Treatments include antacids, H2 blockers, proton pump inhibitors (PPIs), prostaglandin analogues, and cytoprotective agents.

120
Q

What is the treatment regimen for H. pylori associated with gastric ulcers?

A

Triple therapy, which includes two antibiotics plus a PPI for 14 days.

121
Q

What is Zollinger-Ellison syndrome?

A

It’s a condition characterized by a non-beta cell islet tumor of the pancreas, which causes hypersecretion of gastrin.

122
Q

What does gastrin do in Zollinger-Ellison syndrome?

A

Gastrin stimulates excessive gastric acid secretion.

123
Q

How does the feedback mechanism work in Zollinger-Ellison syndrome?

A

The normal negative feedback loop, where gastric acid inhibits further gastrin release, is absent in ZE syndrome.

124
Q

What are the symptoms of Zollinger-Ellison syndrome?

A

Symptoms include peptic ulcer disease, erosive esophagitis, and diarrhea.

125
Q

What percentage of peptic ulcer disease patients have Zollinger-Ellison syndrome?

A

Occurs in 0.1-1% of peptic ulcer disease patients.

126
Q

Who is most commonly affected by Zollinger-Ellison syndrome?

A

More common in males than females; most commonly between ages 30-50.

127
Q

What percent of patients with gastrinomas are metastatic at time of diagnosis?

A

Up to 50% of patients with gastrinomas are metastatic at the time of diagnosis.

128
Q

What is the treatment for Zollinger-Ellison syndrome?

A

Treatment includes proton pump inhibitors and surgical resection of the gastrinoma.

129
Q

What complications are associated with Zollinger-Ellison syndrome that need to be managed preoperatively?

A

Patients may have increased gastric fluid volume, potential electrolyte imbalances, and endocrine abnormalities.

Preoperatively, electrolytes should be corrected, gastric pH increased with medications, and rapid sequence induction (RSI) used.

130
Q

What is the role of small intestinal motility?

A

It mixes stomach contents with digestive enzymes, further reducing particle size and increasing solubility for digestion.

131
Q

What is the major function of the small intestine?

A

To circulate contents and expose them to the mucosal wall to maximize absorption of water, nutrients, and vitamins.

132
Q

How do the muscle layers of the small intestine contribute to its function?

A

The circular and longitudinal muscle layers coordinate to achieve segmentation, aiding in the digestive process.

133
Q

What is segmentation in the context of the small intestine?

A

Segmentation is the contraction of two nearby areas that isolate a segment of the intestine to aid in absorption.

134
Q

Why is segmentation important in the small intestine?

A

It allows contents to remain in the intestine long enough for essential substances to be absorbed into circulation.

135
Q

What controls segmentation in the small intestine?

A

Segmentation is controlled mainly by the enteric nervous system, with modulation by the extrinsic nervous system.

136
Q

What are some reversible causes of small bowel dysmotility?

A
  • Mechanical obstructions (e.g., hernias, malignancy, adhesions, volvulus)
  • Bacterial overgrowth affecting absorptive function
  • Ileus
  • Electrolyte imbalances
  • Critical illness impacting bowel function
137
Q

What are nonreversible causes of small bowel dysmotility, and how are they classified?

A
  • Structural causes like scleroderma, connective tissue disorders, inflammatory bowel disease (IBD)
  • Neuropathic causes such as chronic intestinal pseudo-obstruction, where there is a disruption in the intrinsic and extrinsic nervous systems leading to weak, uncoordinated intestinal contractions
138
Q

What symptoms are associated with small bowel dysmotility?

A
  • Bloating
  • Nausea
  • Vomiting
  • Abdominal pain
139
Q

What are the primary functions of the large intestine?

A
  • Acts as a reservoir for waste and indigestible material before elimination.
  • Extracts remaining electrolytes and water from the intestinal contents.
140
Q

How does distention of the ileum and cecum regulate the ileocecal valve?

A

Distention of the ileum relaxes the ileocecal valve, allowing contents to enter the colon.
Cecal distention subsequently contracts the ileocecal valve to prevent backflow.

141
Q

What is the role of giant migrating complexes in the colon?

A
  • They produce mass movements that propel contents across the large intestine.
  • These complexes typically occur 6-10 times a day in a healthy state.
142
Q

What are the primary symptoms associated with colonic dysmotility?

A
  • Altered bowel habits (e.g., constipation, diarrhea)
  • Intermittent abdominal cramping
143
Q

Which are the most common diseases associated with colonic dysmotility?

A

Irritable Bowel Syndrome (IBS)
Inflammatory Bowel Disease (IBD)

144
Q

What does the Rome II criteria specify for the diagnosis of IBS?

A
  • Discomfort is relieved by defecation.
  • Onset is associated with a change in frequency of stool (> 3 times per day or < 3 times per week).
  • Onset is associated with a change in form (appearance) of stool.
145
Q

How does IBD affect colonic motility?

A
  • supresses normal contractions due to colonic wall compression by inflamed mucosa.
  • Giant migrating complexes remain active, with increased frequency and pressure-effect, which can compress the inflamed mucosa further, leading to potential hemorrhage, thick mucus secretion, and significant erosions.
146
Q

What is the incidence of Inflammatory Bowel Disease (IBD)?

A

The incidence of IBD is 18 per 100,000 people.

It is the 2nd most common inflammatory disorder after RA.

147
Q

Describe the characteristics of Ulcerative Colitis (UC).

A
  • Mucosal disease of the rectum and part or all of the colon.
  • In severe cases, the mucosa is hemorrhagic, edematous, and ulcerated.
148
Q

What are the symptoms of Ulcerative Colitis?

A

Diarrhea, rectal bleeding, crampy abdominal pain, nausea/vomiting, fever, weight loss.

149
Q

What laboratory findings are common in Ulcerative Colitis?

A

thrombocytosis

increased erythrocyte sedimentation rate (ESR)

decreased hemoglobin and hematocrit (anemia)

decreased albumin

150
Q

When is surgical colectomy warranted in Ulcerative Colitis?

A

Hemorrhage requiring more than 6 units of blood transfusion within 24-48 hours

151
Q

What are some complications associated with Ulcerative Colitis?

A
  • Toxic megacolon, which is often triggered by electrolyte disturbances and may resolve or require colectomy.
  • Colon perforation, a dangerous complication with a mortality rate of 15%.
152
Q

What is the scope of inflammation in Crohn’s disease and where is it most commonly found?

A
  • It is an acute or chronic inflammatory process that can affect any or all parts of the bowel.
  • The most common site is the terminal ileum, often presenting with ileocolitis, right lower quadrant (RLQ) pain, and diarrhea.
153
Q

What are the two patterns of disease in Crohn’s Disease?

A
  • Penetrating-fistulous disease pattern
  • Obstructing disease pattern
154
Q

What are some of the symptoms associated with Crohn’s Disease?

A
  • Weight loss
  • Fear of eating
  • Anorexia
  • Diarrhea
155
Q

What happens to the bowel as Crohn’s Disease progresses?

A
  • Persistent inflammation can lead to fibrous narrowing and stricture formation.
  • Initially frequent diarrhea may decrease, replaced by symptoms of chronic bowel obstruction.
  • Extensive inflammation may result in loss of absorptive surfaces, leading to malabsorption and steatorrhea.
156
Q

What are some complications of colonic disease in Crohn’s?

A

Colonic disease may fistulize into the stomach or duodenum, potentially causing fecal vomitus.

157
Q

What are some additional symptoms patients with Crohn’s Disease may experience?

A
  • Arthritis
  • Dermatitis
  • Kidney stones
158
Q

What is the mainstay of medical treatment for Inflammatory Bowel Disease (IBD)?

A

5-Acetylsalicylic acid (5-ASA) due to its antibacterial and anti-inflammatory properties.

It’s not aspirin (ASA)

159
Q

What medications are used during flare-ups of IBD?

A

Oral or IV Glucocorticoids.

160
Q

Which antibiotics are commonly prescribed for IBD?

A

Rifaximin
Metronidazole (Flagyl)
Ciprofloxacin (Cipro)

161
Q

What is the role of purine analogues in the treatment of IBD?

A

Purine analogues are used in the management of IBD, although the card doesn’t specify the particular purine analogues or their mechanisms of action.

162
Q

When is surgery considered for IBD and what are the guidelines for intestinal resection?

A

Surgery is considered a last resort for IBD.
The resected segment should be as conservative as possible.
Small intestine resection should be limited to less than half the total length to avoid short bowel syndrome.

163
Q

What happens if more than two-thirds of the small intestine is resected?

A

Resection of more than two-thirds of the small intestine leads to short bowel syndrome, which may require total parenteral nutrition (TPN).

164
Q

Where do most carcinoid tumors originate in the body?

A

Most carcinoid tumors originate from the gastrointestinal (GI) tract and may occur in any segment or tissue of the GI system.

165
Q

What substances do carcinoid tumors secrete?

A

Peptides and vasoactive substances including:
gastrin
insuln
somatostatin
motilin
neurotensin
tachykinins
glucagon
serotonin
and other biologically active substances.

166
Q

In what percentage of patients with carcinoid tumors does carcinoid syndrome occur?

A

Carcinoid Syndrome occurs in approximately 10% of patients with carcinoid tumors.

167
Q

What are the symptoms of Carcinoid Syndrome?

A
  • Flushing
  • Diarrhea
  • Hypertension or Hypotension (HTN/HoTN)
  • Bronchoconstriction
168
Q

How does Carcinoid Syndrome affect the heart?

A
  • It may lead to right heart endocardial fibrosis.
  • The left heart is generally more protected due to the lungs clearing some of the vasoactive substances.
169
Q

How is Carcinoid Syndrome diagnosed?

A

Measuring urinary or plasma serotonin levels.
Imaging with CT or MRI.

170
Q

How does Carcinoid Syndrome develop in patients?

A

Large amounts of serotonin and vasoactive substances reach the systemic circulation, leading to the symptoms of the syndrome.

171
Q

What are the symptoms of Carcinoid Syndrome?

A
  • Flushing
  • Diarrhea
  • Hypertension (HTN) or Hypotension (HoTN)
  • Bronchoconstriction
172
Q

What cardiac condition may be acquired due to Carcinoid Syndrome?

A

Right heart endocardial fibrosis, while the left heart is generally more protected as the lungs clear some of the vasoactive substances.

173
Q

What are the treatment strategies for Carcinoid Syndrome?

A
  • Avoid triggers that increase serotonin.
  • Control diarrhea.
  • Use serotonin antagonists and somatostatin analogues.
174
Q

What preoperative management is advised for patients with carcinoid tumors?

A

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

175
Q

Carcinoid tumors video

A

https://www.youtube.com/watch?v=ndfdIOzATjc

176
Q

Secretory Characteristics of Carcinoid Tumors in Various Sites chart

A

Midgut - secretes high amounts of serotonin and tachykinins

Rarely 5-HTP and ACTH

177
Q

Location and Presentation of Carcinoid tumors

A
178
Q

What is pancreatitis?

A

Pancreatitis is an inflammatory disorder of the pancreas.

179
Q

How has the incidence of pancreatitis changed since the 1960s?

A

The incidence of pancreatitis has increased tenfold since the 1960s, likely due to increased alcoholism and improved diagnostics.

180
Q

How is autodigestion normally prevented in the pancreas?

A
  • Proteases are packaged in their precursor form.
  • Presence of protease inhibitors.
  • Low intra-pancreatic calcium levels, which decrease trypsin activity.
181
Q

What are the most common causes of pancreatitis?

A

Gallstones and alcohol abuse are the most common causes, accounting for 60-80% of cases.

182
Q

How do gallstones lead to pancreatitis?

A

Gallstones obstruct the ampulla of Vater, causing pancreatic ductal hypertension.

183
Q

What other conditions are associated with pancreatitis?

A
  • Immunodeficiency syndrome
  • Hyperparathyroidism or elevated calcium levels (hypercalcemia)
184
Q

What are the common symptoms of pancreatitis?

A
  • Excruciating epigastric pain radiating to the back
  • Nausea and vomiting (N/V)
  • Abdominal distention
  • Steatorrhea
  • Ileus
  • Fever
  • Tachycardia
  • Hypotension (HoTN)
185
Q

What are the hallmark laboratory findings in pancreatitis?

A

Elevated serum amylase and lipase levels.

186
Q

What imaging techniques are used for diagnosing pancreatitis?

A
  • Contrast-enhanced computed tomography (CT) or magnetic resonance imaging (MRI)
  • Endoscopic ultrasound (EUS)
187
Q

What are some serious complications associated with pancreatitis?

A

Shock
Acute respiratory distress syndrome (ARDS)
Renal failure
Necrotic pancreatic abscess

188
Q

What are the initial treatment steps for pancreatitis?

A
  • Aggressive intravenous fluids (IVF)
  • Nil per os (NPO) to rest the pancreas
  • Enteral feeding is preferred over total parenteral nutrition (TPN) due to the risk of infectious complications with TPN
  • Opioids for pain management
189
Q

What is ERCP and what are its indications?

A
  • Endoscopic retrograde cholangiopancreatography (ERCP) is a fluoroscopic examination of the biliary and pancreatic ducts.
  • Interventions include stone removal, stent placement, sphincterotomy, and hemostasis.
190
Q

How does the prevalence of upper GI bleeding compare to lower GI bleeding?

A

Upper GI bleeding is more common than lower GI bleeding.

191
Q

What are the signs that indicate more than 25% blood loss in GI bleeding?

A

Hypotension (HoTN) and tachycardia are signs that may indicate more than 25% blood loss.

192
Q

What does orthostatic hypotension normally indicate about hematocrit (HCT) levels?

A

Orthostatic hypotension normally indicates a hematocrit level below 30%.

193
Q

What does the presence of melena indicate about the location of a GI bleed?

A

Melena indicates that the bleed is above the cecum (where the small intestine meets the colon).

194
Q

What BUN levels are typically seen in upper GI bleeding, and why?

A

Blood Urea Nitrogen (BUN) typically exceeds 40 mg/dL due to absorbed nitrogen into the bloodstream from the site of bleeding.

195
Q

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

A

Esophagogastroduodenoscopy (EGD) is the diagnostic and therapeutic procedure of choice.

196
Q

What endoscopic interventions can be performed for upper GI bleeding?

A

Endoscopic ulcer ligation (with a perforation treatment rate of 0.5%).
Ligation of bleeding varices.

197
Q

What is the last resort intervention for uncontrolled variceal bleeding?

A

Mechanical balloon tamponade.

198
Q

Who is most commonly affected by lower GI bleeding?

A

Lower GI bleeding generally occurs in the elderly.

199
Q

What are the common causes of lower GI bleeding?

A

Diverticulosis
Tumors
Colitis

200
Q

What is the initial diagnostic procedure for lower GI bleeding upon stabilization?

A

An unprepped sigmoidoscopy is performed as soon as the patient is hemodynamically stable.

201
Q

When is a colonoscopy performed for lower GI bleeding?

A

A colonoscopy is performed if the patient can tolerate the preparatory procedure.

202
Q

What intervention is warranted for persistent lower GI bleeding?

A

Persistent bleeding warrants angiography and potential embolic therapy.

203
Q

What characterizes colonic ileus?

A

Colonic ileus is characterized by massive dilation of the colon without mechanical obstruction, leading to loss of peristalsis and colonic distention.

204
Q

What can cause colonic ileus?

A

Possible causes include

  • electrolyte disorders,
  • immobility,
  • excessive use of narcotics or anticholinergic drugs, and an
  • imbalance of neural input with excessive sympathetic and inadequate parasympathetic stimulation to the colon.
205
Q

What are the treatment strategies for colonic ileus?

A

Treatments include restoring electrolyte balance, hydration, mobilization, nasogastric (NG) suction, and enemas.

206
Q

What is the role of neostigmine in the treatment of colonic ileus, and what monitoring is required?

A

Neostigmine (AChE-i - increases ACh activity, thus stimulating the PNS and improving GI function) administered at 2-2.5 mg over 5 minutes can produce immediate results in 80-90% of cases. Cardiac monitoring is required due to potential bradycardia.

207
Q

What risks are associated with untreated colonic ileus?

A

If left untreated, colonic ileus may lead to ischemia and potential perforation of the colon.

208
Q

What is the typical state of preoperative patients?

A

Nervous and sympathetically charged.

209
Q

What happens to GI activity with increased anxiety in preoperative patients?

A

It is inhibited, proportional to the amount of norepinephrine secreted from sympathetic nervous system stimulation.

210
Q

What effect do volatile anesthetics have on the activity of the stomach, small intestine, and colon?

A

They depress spontaneous, electrical, contractile, and propulsive activity in these organs.

211
Q

In what order do the parts of the GI tract recover postoperatively?

A

The small intestine recovers first, followed by the stomach within approximately 24 hours, and then the colon within 30 to 40 hours.

212
Q

How do volatile agents, coupled with surgery-induced sympathetic hyperactivity, affect GI function and motility?

A

They inhibit GI function and motility.

213
Q

What is the relative solubility of nitrous oxide compared to nitrogen in the blood?

A

Nitrous oxide is 30 times more soluble than nitrogen in the blood.

214
Q

How does nitrous oxide affect gas-containing cavities in the body?

A

It diffuses into gas-containing cavities from the blood faster than nitrogen can diffuse out.

215
Q

What factors correlate with gut distention during nitrous oxide administration?

A

Pre-existing gas in the bowel, duration of nitrous oxide administration, and concentration of nitrous oxide administered.

216
Q

When should nitrous oxide be avoided in surgical procedures?

A

In lengthy abdominal surgeries or when the bowel is already distended.

217
Q

```

What is the effect of neuromuscular blockers (NMBs) on gastrointestinal motility?

A

NMBs only affect skeletal muscle, leaving GI motility intact.

218
Q

How does Neostigmine (AchE-I) affect parasympathetic nervous system (PNS) activity and bowel peristalsis?

A

It increases PNS activity and bowel peristalsis by increasing the frequency and intensity of contractions.

219
Q

What is the purpose of concurrent administration of anticholinergic medications (glycopyrrolate or atropine) with Neostigmine?

A

To counteract the bradycardia associated with Neostigmine.

Increased PNS activity also means that the heart’s PNS activity will increase thus causing a drop in HR

220
Q

What effect does the alternate reversal agent, Sugammadex, have on bowel motility?

A

Sugammadex does not appear to have any effect on motility.

221
Q

What effect do opioids have on gastrointestinal (GI) motility?

A

Opioids cause reduced GI motility and constipation.

222
Q

Where do opioids exert their function?

A

Opioids exert their function on both central and peripheral mu, delta, and kappa receptors.

223
Q

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

A

In the myenteric and submucosal plexuses.

224
Q

What is the result of activation of mu-receptors in the GI tract?

A

Activation of mu-receptors causes delayed gastric emptying and slower transit through the intestine.

225
Q

What are some other adverse events associated with opioid use in the GI tract?

A

Nausea, anorexia, delayed digestion, abdominal pain, excessive straining during bowel movements, and incomplete evacuation.

226
Q

Key Points Slide

A
227
Q

Key Points Slide 2

A

Assessment '24 - Mordecai (10 decks)

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