T4 - GI Assessment Flashcards
1
Q
What percentage of the total human body mass does the GI tract constitute?
A
Approximately 5%.
2
Q
What are the main functions of the GI tract?
A
Motility, digestion, absorption, excretion, and circulation.
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.
4
Q
What are the components within the mucosa from outermost to innermost?
A
Muscularis mucosae, lamina propria, and epithelium.
5
Q
What is the function of the serosa?
A
It is a smooth membrane of thin connective tissue and cells that secrete serous fluid to enclose the cavity and reduce friction between muscle movements.
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.
7
Q
What does the circular muscle layer do?
A
It contracts to decrease the diameter of the intestinal lumen.
8
Q
How do the longitudinal and circular muscle layers work together?
A
They work together to propagate gut motility.
9
Q
Which plexus supplies innervation to the GI organs up to the proximal transverse colon?
A
The celiac plexus.
10
Q
Where does the innervation of the descending colon and distal GI tract come from?
A
The inferior hypogastric plexus.
11
Q
What are some of the approaches to block the celiac plexus?
A
- Transcrural
- Intraoperative
- Endoscopic ultrasound-guided
- Peritoneal lavage
12
Q
Where is the myenteric plexus located and what is its function?
A
The myenteric plexus is situated between the smooth muscle layers and regulates their function.
13
Q
What is the role of the submucosal plexus in the GI tract?
A
The submucosal plexus transmits information from the epithelium to the enteric and central nervous systems.
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.
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.
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.
17
Q
What are the components of the GI tract’s autonomic nervous system (ANS)?
A
*extrinsic nervous system: SNS and PSNS
*enteric nervous system.
18
Q
What is the primary function of the extrinsic SNS in the GI tract?
A
It is primarily inhibitory and decreases GI motility.
19
Q
How does the extrinsic PNS affect the GI tract?
A
It is primarily excitatory and activates GI motility.
20
Q
What does the enteric nervous system control?
A
It independently controls motility, secretion, and blood flow within the GI tract.
21
Q
What is the enteric system comprised of?
A
The myenteric plexus and submucosal plexus.
22
Q
What functions are regulated by the submucosal plexus?
A
Absorption, secretion, and mucosal blood flow.
23
Q
How do the myenteric and submucosal plexuses respond to stimulation?
A
They respond to both sympathetic and parasympathetic stimulation.
24
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.
25
What are some anesthesia challenges during an Upper Gastrointestinal Endoscopy?
Sharing the airway
performing the procedure outside of the main OR.
26
What are some anesthesia challenges during a Colonoscopy?
Patient dehydration due to bowel preparation and NPO (nil per os, nothing by mouth) status.
27
What does High Resolution Manometry (HRM) measure?
HRM measures pressures along the entire length of the esophagus.
28
What is HRM generally used to diagnose?
Motility disorders of the esophagus.
29
What is a GI series with ingested barium used for?
It is a radiologic assessment of swallowing function and GI transit.
30
How is a gastric emptying study conducted?
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.
31
What does small intestine manometry measure?
It measures contraction pressures and motility of the small intestine.
32
How are contractions evaluated during small intestine manometry?
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.
33
What does a lower GI series involve and what does it detect?
It involves the administration of a barium enema to outline the intestines on radiographs, allowing for the detection of colon and rectal anatomical abnormalities.
34
Into what categories are diseases of the esophagus grouped?
Anatomical
Mechanical
Neurologic
Although many disease states overlap
35
What are some anatomical causes of esophageal diseases?
Diverticula
hiatal hernia
changes associated with chronic acid reflux
36
What are mechanical causes of esophageal diseases?
Achalasia (failure of smooth muscle fibers to relax)
esophageal spasms
hypertensive lower esophageal sphincter (LES).
37
What can neurologic causes of esophageal diseases be a result of?
stroke
vagotomy
hormone deficiencies.
38
What are the most common symptoms of esophageal disease?
Dysphagia, heartburn, and GERD (Gastroesophageal Reflux Disease).
39
What is dysphagia and how is it classified?
Dysphagia is difficulty swallowing, which may be oropharyngeal or esophageal.
40
What is a common cause of oropharyngeal dysphagia?
It's commonly seen after head and neck surgeries.
41
How can esophageal dysphagia be categorized based on physiology?
(mechanical vs. esophageal)
* Esophageal dysmotility: Symptoms occur with both liquids and solids.
* Mechanical esophageal dysphasia: Symptoms only occur with solid food.
42
What is GERD and what are its common symptoms?
GERD is the effortless return of gastric contents into the pharynx, often causing heartburn, nausea, and a sensation of a "lump in the throat."
43
What is achalasia?
Achalasia is a neuromuscular disorder of the esophagus characterized by inadequate LES tone leading to outflow obstruction, and a dilated, hypomobile esophagus.
44
What causes achalasia?
The loss of ganglionic cells in the esophageal myenteric plexus, absence of inhibitory neurotransmitters of the LES, and unopposed cholinergic LES stimulation preventing relaxation.
45
What are the symptoms of achalasia?
Dysphagia, regurgitation, heartburn, and chest pain.
46
How is achalasia diagnosed?
With esophageal manometry and/or esophagram.
47
What are the three classes of achalasia and how do they respond to treatment?
* 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.
48
What medications are used for achalasia treatment?
Nitrates and calcium channel blockers (CCBs) to relax the lower esophageal sphincter (LES).
49
What endoscopic treatment is used for achalasia?
Endoscopic botox injections to temporarily relax the LES.
50
Which non-surgical treatment is most effective for achalasia?
Pneumatic dilation.
51
What is considered the best surgical treatment for achalasia?
Laparoscopic Heller Myotomy.
52
What is a Peri-oral Endoscopic Myotomy (POEM) and its risks?
POEM is an endoscopic division of LES muscle layers with a 40% risk of developing pneumothorax or pneumoperitoneum.
53
What is the anesthesia consideration for patients with achalasia?
Patients are at increased risk for aspiration; Rapid Sequence Induction (RSI) or awake intubation is indicated.
54
What are Diffuse Esophageal Spasms and where do they commonly occur?
Spasms that usually occur in the distal esophagus and are likely due to autonomic dysfunction.
55
Who is more commonly affected by Diffuse Esophageal Spasms?
the elderly.
56
How is Diffuse Esophageal Spasm diagnosed?
Diagnosed on an esophagram.
57
What can the pain from Diffuse Esophageal Spasms mimic?
Pain can mimic angina.
58
What are some treatments for Diffuse Esophageal Spasms?
Treatments include nitroglycerin (NTG), antidepressants, and phosphodiesterase inhibitors (PD-Is).
59
What are Esophageal Diverticula?
Outpouchings in the wall of the esophagus.
60
What is Pharyngoesophageal (Zenker) Diverticulum and a symptom associated with it?
A type of esophageal diverticulum associated with bad breath due to food retention.
61
What might cause Midesophageal Diverticula?
May be caused by old adhesions or inflamed lymph nodes.
62
What condition may patients with Epiphrenic (supradiaphragmatic) Diverticula also experience?
Patients may also experience achalasia.
63
What is a Hiatal Hernia?
A herniation of the stomach into the thoracic cavity through the esophageal hiatus in the diaphragm.
64
What can cause a Hiatal Hernia?
It can be caused by weakening in the anchors of the gastroesophageal (GE) junction to the diaphragm.
65
What are common symptoms associated with a Hiatal Hernia?
It may be asymptomatic but is often associated with GERD (Gastroesophageal Reflux Disease).
66
How does esophageal cancer typically present?
With progressive dysphagia and weight loss.
67
Why is the survival rate poor for esophageal cancer?
Because the abundant lymphatics lead to lymph node metastasis.
68
What are the risk factors for esophageal cancer?
GERD
Barrett's esophagus
obesity.
69
What types of cancer account for esophageal cancers?
adenocarcinomas (most common)
Squamous cell carcinoma.
70
How can an esophagectomy be performed?
It may be performed transthoracically, transhiatally, or using minimally invasive techniques.
71
What is a common complication of esophagectomy and its prognosis?
High risk of recurrent laryngeal nerve injury, with about 40% resolving spontaneously.
72
What nutritional status is common in patients preoperatively and post-esophagectomy?
Patients often present malnourished before the operation and may remain so for many months after.
73
What complications may present if there is a history of chemotherapy or radiation prior to esophagectomy?
Pancytopenia and dehydration.
74
What is a long-term risk for patients after esophagectomy?
They are at a very high risk for aspiration for life.
75
What causes GERD?
Incompetence of the gastroesophageal junction, leading to reflux.
76
What are common symptoms of GERD?
Heartburn, dysphagia, and mucosal injury.
77
Prevalence of GERD in adults?
Occurs in 15% of adults.
78
What does reflux content include in GERD?
Hydrochloric acid (HCl), pepsin, pancreatic enzymes, and bile.
79
How is bile reflux associated with Barrett metaplasia and adenocarcinoma?
Bile reflux is associated with Barrett metaplasia and an increased risk of adenocarcinoma.
80
What are the three mechanisms of gastroesophageal incompetence in GERD?
* 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.
81
What lifestyle intervention is recommended for GERD treatment?
Avoidance of trigger foods.
82
What medications are commonly used for GERD?
Antacids, H2 blockers, and Proton Pump Inhibitors (PPIs).
83
What are some surgical options for GERD?
Nissen Fundoplication, Toupet fundoplication, and LINX device placement.
84
What preoperative interventions are used for GERD patients?
* Cimetidine and Ranitidine to decrease acid secretion and increase pH.
* PPIs generally given the night before and the morning of surgery.
* Sodium Citrate, an oral nonparticulate antacid.
85
What medication can be given to enhance gastric emptying?
Metoclopramide, which is a gastrokinetic; often reserved for diabetics, obese, and pregnant patients.
86
Factors that increase intra-op aspiration risk:
* Emergent surgery
* Full Stomach
* Difficult airway
* Inadequate anesthesia depth
* Lithotomy
* Autonomic Neuropathy
* Gastroparesis
* DM
* Pregnancy
* ↑ Intraabdominal pressure
* Severe Illness
* Morbid Obesity
87
What size must solids be broken down into before entering the duodenum?
Solids must be broken down into 1-2 mm particles.
88
What regulates the motility of the stomach?
Motility is controlled by both intrinsic and extrinsic neural regulation.
89
How does parasympathetic stimulation affect stomach contractions?
It increases the number and force of contractions via the vagus nerve.
90
What is the effect of sympathetic stimulation on stomach contractions?
It inhibits these contractions via the splanchnic nerve.
91
What provides coordination for stomach motility?
The intrinsic nervous system.
92
Which substances are involved in neurohormonal control of stomach motility and how do they affect it?
* Gastrin and motilin increase the strength and frequency of contractions.
* Gastric inhibitory peptide inhibits contractions.
93
What is often associated with Peptic Ulcer Disease?
Helicobacter pylori infection.
94
What are common symptoms of Peptic Ulcer Disease?
Burning epigastric pain that is exacerbated with fasting and improved with meals.
95
What is the risk of perforation in Peptic Ulcer Disease without treatment?
There is a 10% risk of perforation.
96
What are the signs of a perforated peptic ulcer?
Sudden and severe epigastric pain due to acidic secretions entering the peritoneum.
97
What are common causes of mortality in Peptic Ulcer Disease?
Mortality is due to shock or perforation if untreated for more than 48 hours.
98
What is gastric outlet obstruction?
Gastric outlet obstruction is a blockage that prevents food from leaving the stomach and entering the small intestine.
99
What are potential causes of gastric outlet obstruction?
Causes can include peptic ulcers, malignancies, gastric polyps, or strictures following inflammation.
100
What are common symptoms of gastric outlet obstruction?
Symptoms often include vomiting, abdominal pain, bloating, and a reduced appetite.
101
How is gastric outlet obstruction diagnosed?
It can be diagnosed using imaging studies like an upper gastrointestinal series or endoscopy.
102
What treatments are available for gastric outlet obstruction?
Treatments may involve endoscopic procedures to remove the obstruction, surgical intervention, or medications to reduce inflammation and promote healing.
103
How many types of gastric ulcers are there?
There are five types of gastric ulcers.
104
What are common causes of gastric ulcers?
They are commonly caused by excessive use of NSAIDs, infection with H. pylori, and alcohol consumption (ETOH).
105
What are the treatments for gastric ulcers?
Treatments include antacids, H2 blockers, proton pump inhibitors (PPIs), prostaglandin analogues, and cytoprotective agents.
106
What is the treatment regimen for H. pylori associated with gastric ulcers?
Triple therapy, which includes two antibiotics plus a PPI for 14 days.
107
What is Zollinger-Ellison syndrome?
It's a condition characterized by a non-beta cell islet tumor of the pancreas, which causes hypersecretion of gastrin --> excessive gastric acid secretion
108
How does the feedback mechanism work in Zollinger-Ellison syndrome?
The normal negative feedback loop, where gastric acid inhibits further gastrin release, is absent in ZE syndrome.
109
What are the symptoms of Zollinger-Ellison syndrome?
Symptoms include peptic ulcer disease, erosive esophagitis, and diarrhea.
110
Who is most commonly affected by Zollinger-Ellison syndrome?
More common in males than females; most commonly between ages 30-50.
111
What is the treatment for Zollinger-Ellison syndrome?
Treatment includes proton pump inhibitors and surgical resection of the gastrinoma.
112
What complications are associated with Zollinger-Ellison syndrome that need to be managed preoperatively?
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.
113
Why is segmentation important in the small intestine?
It allows contents to remain in the intestine long enough for essential substances to be absorbed into circulation.
114
What controls segmentation in the small intestine?
Segmentation is controlled mainly by the enteric nervous system, with modulation by the extrinsic nervous system.
115
What are some reversible causes of small bowel dysmotility?
* Mechanical obstructions (e.g., hernias, malignancy, adhesions, volvulus)
* Bacterial overgrowth affecting absorptive function
* Ileus
* Electrolyte imbalances
* Critical illness impacting bowel function
116
What are nonreversible causes of small bowel dysmotility, and how are they classified?
* 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
117
What symptoms are associated with small bowel dysmotility?
* Bloating
* Nausea
* Vomiting
* Abdominal pain
118
What are the primary functions of the large intestine?
* Acts as a reservoir for waste and indigestible material before elimination.
* Extracts remaining electrolytes and water from the intestinal contents.
119
How does distention of the ileum and cecum regulate the ileocecal valve?
Distention of the ileum relaxes the ileocecal valve, allowing contents to enter the colon.
Cecal distention subsequently contracts the ileocecal valve to prevent backflow.
120
What is the role of giant migrating complexes in the colon?
* They produce mass movements that propel contents across the large intestine.
* These complexes typically occur 6-10 times a day in a healthy state.
121
What are the primary symptoms associated with colonic dysmotility?
* Altered bowel habits (e.g., constipation, diarrhea)
* Intermittent abdominal cramping
122
Which are the most common diseases associated with colonic dysmotility?
Irritable Bowel Syndrome (IBS)
Inflammatory Bowel Disease (IBD)
123
What does the Rome II criteria specify for the diagnosis of IBS?
* 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.
124
How does IBD affect colonic motility?
* In IBD, normal contractions are suppressed 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.
125
What is the incidence of Inflammatory Bowel Disease (IBD)?
It is the 2nd most common inflammatory disorder after RA.
126
Describe the characteristics of Ulcerative Colitis (UC).
* Mucosal disease of the rectum and part or all of the colon.
* In severe cases, the mucosa is hemorrhagic, edematous, and ulcerated.
127
What are the symptoms of Ulcerative Colitis?
Diarrhea, rectal bleeding, crampy abdominal pain, nausea/vomiting, fever, weight loss.
128
What laboratory findings are common in Ulcerative Colitis?
* May have increased platelets (thrombocytosis)
* increased erythrocyte sedimentation rate (ESR),
* decreased hemoglobin and hematocrit (anemia),
* decreased albumin.
129
When is surgical colectomy warranted in Ulcerative Colitis?
Hemorrhage requiring more than 6 units of blood transfusion within 24-48 hours
130
What are some complications associated with Ulcerative Colitis?
* 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%.
131
What is the scope of inflammation in Crohn's disease and where is it most commonly found?
* 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.
132
What are the two patterns of disease in Crohn's Disease?
* Penetrating-fistulous disease pattern
* Obstructing disease pattern
133
What are some of the symptoms associated with Crohn's Disease?
* Weight loss
* Fear of eating
* Anorexia
* Diarrhea
134
What happens to the bowel as Crohn's Disease progresses?
* 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.
135
What are some complications of colonic disease in Crohn's?
Colonic disease may fistulize into the stomach or duodenum, potentially causing fecal vomitus.
136
What are some additional symptoms patients with Crohn’s Disease may experience?
* Arthritis
* Dermatitis
* Kidney stones
137
What is the mainstay of medical treatment for Inflammatory Bowel Disease (IBD)?
5-Acetylsalicylic acid (5-ASA) due to its antibacterial and anti-inflammatory properties.
138
What medications are used during flare-ups of IBD?
Oral or IV Glucocorticoids.
139
Which antibiotics are commonly prescribed for IBD?
Rifaximin
Metronidazole (Flagyl)
Ciprofloxacin (Cipro)
140
What is the role of purine analogues in the treatment of IBD?
Purine analogues are used in the management of IBD, although the card doesn't specify the particular purine analogues or their mechanisms of action.
141
When is surgery considered for IBD and what are the guidelines for intestinal resection?
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.
142
What happens if more than two-thirds of the small intestine is resected?
Resection of more than two-thirds of the small intestine leads to short bowel syndrome, which may require total parenteral nutrition (TPN).
143
Where do most carcinoid tumors originate in the body?
Most carcinoid tumors originate from the gastrointestinal (GI) tract and may occur in any segment or tissue of the GI system.
144
What substances do carcinoid tumors secrete?
Peptides and vasoactive substances including gastrin, insulin, somatostatin, motilin, neurotensin, tachykinins, glucagon, serotonin, and other biologically active substances.
145
In what percentage of patients with carcinoid tumors does carcinoid syndrome occur?
Carcinoid Syndrome occurs in approximately 10% of patients with carcinoid tumors.
146
What are the symptoms of Carcinoid Syndrome?
* Flushing
* Diarrhea
* Hypertension or Hypotension (HTN/HoTN)
* Bronchoconstriction
147
How does Carcinoid Syndrome affect the heart?
* 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.
148
How is Carcinoid Syndrome diagnosed?
Measuring urinary or plasma serotonin levels.
Imaging with CT or MRI.
149
How does Carcinoid Syndrome develop in patients?
Large amounts of serotonin and vasoactive substances reach the systemic circulation, leading to the symptoms of the syndrome.
150
What are the symptoms of Carcinoid Syndrome?
* Flushing
* Diarrhea
* Hypertension (HTN) or Hypotension (HoTN)
* Bronchoconstriction
151
What cardiac condition may be acquired due to Carcinoid Syndrome?
Right heart endocardial fibrosis, while the left heart is generally more protected as the lungs clear some of the vasoactive substances.
152
What are the treatment strategies for Carcinoid Syndrome?
* Avoid triggers that increase serotonin.
* Control diarrhea.
* Use serotonin antagonists and somatostatin analogues.
153
What preoperative management is advised for patients with carcinoid tumors?
Administration of Octreotide before surgery and prior to tumor manipulation to attenuate volatile hemodynamic changes.
154
Secretory Characteristics of Carcinoid Tumors in Various sites chart
155
What is pancreatitis?
Pancreatitis is an inflammatory disorder of the pancreas.
156
How has the incidence of pancreatitis changed since the 1960s?
The incidence of pancreatitis has increased tenfold since the 1960s, likely due to increased alcoholism and improved diagnostics.
157
How is autodigestion normally prevented in the pancreas?
* Proteases are packaged in their precursor form.
* Presence of protease inhibitors.
* Low intra-pancreatic calcium levels, which decrease trypsin activity.
158
What are the most common causes of pancreatitis?
Gallstones and alcohol abuse are the most common causes, accounting for 60-80% of cases.
159
How do gallstones lead to pancreatitis?
Gallstones obstruct the ampulla of Vater, causing pancreatic ductal hypertension.
160
What other conditions are associated with pancreatitis?
* Immunodeficiency syndrome
* Hyperparathyroidism or elevated calcium levels (hypercalcemia)
161
What are the common symptoms of pancreatitis?
* Excruciating epigastric pain radiating to the back
* Nausea and vomiting (N/V)
* Abdominal distention
* Steatorrhea
* Ileus
* Fever
* Tachycardia
* Hypotension (HoTN)
162
What are the hallmark laboratory findings in pancreatitis?
Elevated serum amylase and lipase levels.
163
What imaging techniques are used for diagnosing pancreatitis?
* Contrast-enhanced computed tomography (CT) or magnetic resonance imaging (MRI)
* Endoscopic ultrasound (EUS)
164
hat are some serious complications associated with pancreatitis?
Shock
Acute respiratory distress syndrome (ARDS)
Renal failure
Necrotic pancreatic abscess
165
What are the initial treatment steps for pancreatitis?
* 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
166
What is ERCP and what are its indications?
* ERCP is a fluoroscopic examination of the biliary and pancreatic ducts.
* Interventions include stone removal, stent placement, sphincterotomy, and hemostasis.
167
How does the prevalence of upper GI bleeding compare to lower GI bleeding?
Upper GI bleeding is more common than lower GI bleeding.
168
What are the signs that indicate more than 25% blood loss in GI bleeding?
Hypotension (HoTN) and tachycardia are signs that may indicate more than 25% blood loss.
169
What does orthostatic hypotension normally indicate about hematocrit (HCT) levels?
Orthostatic hypotension normally indicates a hematocrit level below 30%.
170
What does the presence of melena indicate about the location of a GI bleed?
Melena indicates that the bleed is above the cecum (where the small intestine meets the colon).
171
What BUN levels are typically seen in upper GI bleeding, and why?
Blood Urea Nitrogen (BUN) typically exceeds 40 mg/dL due to absorbed nitrogen into the bloodstream from the site of bleeding.
172
What is the diagnostic and therapeutic procedure of choice for upper GI bleeding?
Esophagogastroduodenoscopy (EGD) is the diagnostic and therapeutic procedure of choice.
173
What endoscopic interventions can be performed for upper GI bleeding?
Endoscopic ulcer ligation (with a perforation treatment rate of 0.5%).
Ligation of bleeding varices.
174
What is the last resort intervention for uncontrolled variceal bleeding?
Mechanical balloon tamponade.
175
Who is most commonly affected by lower GI bleeding?
Lower GI bleeding generally occurs in the elderly.
176
What are the common causes of lower GI bleeding?
Diverticulosis
Tumors
Colitis
177
What is the initial diagnostic procedure for lower GI bleeding upon stabilization?
An unprepped sigmoidoscopy is performed as soon as the patient is hemodynamically stable.
178
When is a colonoscopy performed for lower GI bleeding?
A colonoscopy is performed if the patient can tolerate the preparatory procedure.
179
What intervention is warranted for persistent lower GI bleeding?
Persistent bleeding warrants angiography and potential embolic therapy.
180
What characterizes colonic ileus?
Colonic ileus is characterized by massive dilation of the colon without mechanical obstruction, leading to loss of peristalsis and colonic distention.
181
What can cause colonic ileus?
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.
182
What are the treatment strategies for colonic ileus?
Treatments include restoring electrolyte balance, hydration, mobilization, nasogastric (NG) suction, and enemas.
183
What is the role of neostigmine in the treatment of colonic ileus, and what monitoring is required?
Neostigmine 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.
184
What risks are associated with untreated colonic ileus?
If left untreated, colonic ileus may lead to ischemia and potential perforation of the colon.
185
What is the typical state of preoperative patients?
Nervous and sympathetically charged.
186
What happens to GI activity with increased anxiety in preoperative patients?
It is inhibited, proportional to the amount of norepinephrine secreted from sympathetic nervous system stimulation.
187
What effect do volatile anesthetics have on the activity of the stomach, small intestine, and colon?
They depress spontaneous, electrical, contractile, and propulsive activity in these organs.
188
In what order do the parts of the GI tract recover postoperatively?
The small intestine recovers first, followed by the stomach within approximately 24 hours, and then the colon within 30 to 40 hours.
189
How do volatile agents, coupled with surgery-induced sympathetic hyperactivity, affect GI function and motility?
They inhibit GI function and motility.
190
What is the relative solubility of nitrous oxide compared to nitrogen in the blood?
Nitrous oxide is 30 times more soluble than nitrogen in the blood.
191
How does nitrous oxide affect gas-containing cavities in the body?
It diffuses into gas-containing cavities from the blood faster than nitrogen can diffuse out.
192
What factors correlate with gut distention during nitrous oxide administration?
Pre-existing gas in the bowel, duration of nitrous oxide administration, and concentration of nitrous oxide administered.
193
When should nitrous oxide be avoided in surgical procedures?
In lengthy abdominal surgeries or when the bowel is already distended.
194
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What is the effect of neuromuscular blockers (NMBs) on gastrointestinal motility?
NMBs only affect skeletal muscle, leaving GI motility intact.
195
How does Neostigmine (AchE-I) affect parasympathetic nervous system (PNS) activity and bowel peristalsis?
It increases PNS activity and bowel peristalsis by increasing the frequency and intensity of contractions.
196
What is the purpose of concurrent administration of anticholinergic medications (glycopyrrolate or atropine) with Neostigmine?
To counteract the bradycardia associated with Neostigmine.
197
What effect does the alternate reversal agent, Sugammadex, have on bowel motility?
Sugammadex does not appear to have any effect on motility.
198
What effect do opioids have on gastrointestinal (GI) motility?
Opioids cause reduced GI motility and constipation.
199
Where is there a high density of peripheral mu-opioid receptors?
In the myenteric and submucosal plexuses.
200
What is the result of activation of mu-receptors in the GI tract?
Activation of mu-receptors causes delayed gastric emptying and slower transit through the intestine.
201
What are some other adverse events associated with opioid use in the GI tract?
Nausea, anorexia, delayed digestion, abdominal pain, excessive straining during bowel movements, and incomplete evacuation.
