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Health Assessment > Dalani's Deck: Unit 4 - Gastrointestinal > Flashcards

Dalani's Deck: Unit 4 - Gastrointestinal Flashcards

1
Q

How much of total human body mass is the GI tract?

A

5%

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2
Q

What are the 5 main functions of the GI system?

A
  • motility
  • digestion
  • absorption
  • excretion
  • circulation
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3
Q

What are the layers of the GI system from outermost to innermost including the mucosal layers from outermost to innermost?

A

serosa, longitudinal muscle, circular muscle layer, submucosa, mucosa: muscularias mucosae, lamina propria, epithelium

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4
Q

What is the serosa’s function?

A

smooth membrane of thin connective tissue and cells that secrete serous fluid to enclose the cavity and reduce friction between muscle movements

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5
Q

What is the purpose of the longitudinal muscle layer?

A

contracts to shorten the length of the intestinal segment

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6
Q

What is the purpose of the circular muscle layer?

A

contracts to decrease the diameter of the intestinal lumen

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7
Q

What innervates the GI organs up to the proximal transverse colon?

A

celiac plexus

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8
Q

What innervates the descending colon and distal GI tract?

A

inferior hypogastric plexus

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9
Q

What 4 ways can the celiac plexus be blocked?

A
  1. transcrural
  2. intraoperative
  3. endoscopic US guided
  4. peritoneal lavage
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10
Q

Where is the myenteric plexus and what does regulate?

A

between the smooth muscle layers and regulates the smooth muscle

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11
Q

What does the submucosal plexus do?

A

transmits information from the epithelium to the enteric and central nervous system to control absorption, secretion, and mucosal blood flow

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12
Q

What 3 layers make up the mucosa?

A

muscularis mucosa, lamina propria, and epithelium (outermost to innermost)

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13
Q

What does the muscularis mucosa do?

A

it is a thin layer of smooth muscle that functions to move the villi

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14
Q

What is the lamina propria?

A

contains the blood vessels and the nerve endings

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15
Q

What is the function of the GI epithelium?

A

GI contents are sensed, enzymes are secreted, nutrients are absorbed, and waste is secreted

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16
Q

What main system controls the GI tract (both names)?

A

the autonomic nervous system aka the extrinsic nervous system

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17
Q

Which extrinsic system is primarily inhibitory and decreases GI motility?

A

The sympathetic extrinsic system

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18
Q

Which extrinsic system is primarily excitatory and increases GI motility?

A

The parasympathetic extrinsic system

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19
Q

What does the enteric nervous system control?

A

the independent nervous system which controls motility, secretion, and blood flow

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20
Q

What makes up the enteric nervous system?

A

the myenteric plexus and the submucosal plexus

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21
Q

What does the myenteric plexus control?

A

Motility which is carried out by enteric neurons, interstitial cells of Cajal, and smooth muscle cells.

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22
Q

What are the interstitial cells of Cajal also called?

A

the ICC or GI pacemaker cells

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23
Q

Both the submucosal plexus and the myenteric plexus respond to __________ and ___________ stimulation.

A

sympathetic and parasympathetic

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24
Q

What is an upper gastrointestinal endoscopy (EGD)?

A

diagnostic or therapeutic procedure where an endoscope is placed into the esophagus, stomach, pylorus, and duodenum with or without anesthesia

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25
Q

What are the anesthetic challenges associated with EGD?

A

sharing an airway with the endoscopist; procedure is often performed outside of the main OR so we don’t always have all of our equipment

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26
Q

What are the anesthetic challenges associated with colonoscopy?

A

pts are often dehydrated due to bowel prep and NPO status

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27
Q

What is high resolution manometry (HRM)?

A

a pressure catheter measuring pressures alone the entire esophageal length generally used to diagnose motility disorders ; Does not normally require anesthesia

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28
Q

What does GI series with ingested barium show?

A

radiologic assessment of swallowing function and GI transit

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29
Q

What is a gastric emptying study?

A

where a patient fasts for at least 4 hours, then consumes a meal (usually eggs) with a radio-tracer, and the continuous or frequent imaging occurs for the next 1-2 hours to test gastric emptying

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30
Q

What is small intestine manometry?

A

a catheter measures contraction pressures and motility of the small intestine

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31
Q

What 3 periods do we measure contractions during with small intestine manometry?

A

fasting (4 hours), during a meal, post-prandial (2 hrs)

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32
Q

What is a lower GI series?

A

a barium enema to outline the intestine which allows for detection of colon and rectal anatomical abnormaliteis on radiograph

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33
Q

What are the 3 categories of esophageal disease?

A

anatomical, mechanical, neurological

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34
Q

What are anatomical causes of esophageal disease?

A

diverticula, hiatal hernia, changes associated with chronic acid reflux

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35
Q

How do anatomical changes cause esophageal disease?

A

they interrupt the normal pathway of food, which changes the pressure zones of the esophagus

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36
Q

What are mechanical causes of esophageal disease?

A

achalasia, esophageal spasms, hypertensive LES

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37
Q

What are neurologic causes of esophageal disease?

A

neurologic disorders such as stroke, vagotomy, or hormone deficiences

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38
Q

What are the 3 most common symptoms of esophageal disease?

A

dysphagia, heartburn, GERD

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39
Q

When do people usually develop oropharyngeal dysphagia?

A

after head and neck injuries

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40
Q

How do we classify esophageal dysphagia?

A

by physiology; either dysmotility or mechanical

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41
Q

What is esophageal dysmotility?

A

difficulty swallowing both liquids and solids

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42
Q

What is mechanical esophageal dysphagia?

A

difficulty swallowing only solid food

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43
Q

What is GERD?

A

effortless return of gastric contents into pharynx

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44
Q

What is achalasia?

A

neuromuscular disorder of the esophagus consisting of an outflow obstruction due to inadequate LES tone and a dilated hypomobile esophagus

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45
Q

What is achalasia caused by?

A

(theoretically) by a loss of ganglionic cells of the esophageal myenteric plexus followed by absence of inhibitory neurotransmitters of the LES

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46
Q

Achalasia is caused by ____________ LES ____________ (the LES cant relax).

A

unopposed LES stimulation

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47
Q

What are the symptoms of achalasia?

A

dysphagia, regurgitaion, heartburn, chest pain

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48
Q

What does achalasia cause long term?

A

increased risk of esophageal cancer

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49
Q

What is used to diagnose achalasia?

A

esophageal manometry or esophagram

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50
Q

What are the 3 classes of achalasia?

A

1: minimal esophageal pressure, responds well to myotomy;

2: entire esophagus pressurized, responds well to treatment, has the best outcomes;

3: esophageal spasms with premature contractions; has worst outcomes

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51
Q

What medications treat achalasia?

A

nitrates and CCBs to relax LES; endoscopic botox injections

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52
Q

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

A

pneumatic dilation

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53
Q

What is the best surgical treatment for achalasia?

A

Laparoscopic Hellar Myotomy

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54
Q

What is perioral endoscopic myotomy (POEM)?

A

endoscopic division of LES muscle layers

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55
Q

What is the biggest risk to performing POEM?

A

40% of patients develop pneumothorax or pneumoperitoneum

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56
Q

What anesthetic challenges are associated with achalasia?

A

high risk for aspiration; proceed with RSI or awake intubations

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57
Q

What procedure is considered in the most advanced disease states of achalasia?

A

esophagectomy

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58
Q

What are diffuse esophageal spasms?

A

spasms that usually occur in distal esophagus, likely due to autonomic dysfunction, causing pain that mimics angina

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59
Q

What is the diagnosis and treatment of esophageal spasms?

A

diagnosis: esophagram; treatment: nitroglycerin, antidepressants, PD-Is

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60
Q

What population most commonly experiences diffuse esophageal spasms?

A

elderly

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61
Q

What are esophageal diverticula?

A

out-pouchings in the wall of the esophagus

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62
Q

What are Zenker Diverticulum?

A

pharyngoesophageal diverticulum that causes bad breath due to food retention

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63
Q

What is midesophageal diverticulum caused by?

A

old adhesions or inflamed lymph nodes

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64
Q

What is associated with epiphrenic (supradiaphragmatic) diverticula?

A

achalasia

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65
Q

What anesthetic challenges for esophageal diverticula?

A

all aspiration risks; removal of particles and RSI

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66
Q

What is hiatal hernia?

A

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

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67
Q

What causes hiatal hernia?

A

weakening in anchors of gastroesophageal junction to the diaphragm

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68
Q

What is the prevalence of esophageal cancer?

A

4-5 in 100,000 people in the US

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69
Q

How does esophageal cancer present?

A

with progressive dysphagia and weight loss

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70
Q

Why does esophageal cancer have a poor survival rate?

A

because there are abundant lymphatics in esophagus leading to lymph node metastasis

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71
Q

What is the majority of esophageal cancers and what are they related to?

A

adenocarcinomas located in the lower esophagus; related to: GERD, Barretts, Obesity

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72
Q

What are the rest of esophageal cancers (besides adenocarcinomas)?

A

squamous cell carcinoma

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73
Q

How is esophagectomy performed and what are the risks?

A

performed transthoracic, transhiatal, or minimally invasive; HIGH risk of recurrent laryngeal nerve injury of which 40% resolves spontaneously

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74
Q

What symptom is often associated with esophageal cancer preop and for months after treatment?

A

malnourishment

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75
Q

If patients have a history of chemo/radiation, what symptoms may be present?

A

pancytopenia and dehydration

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76
Q

Why are post-esophagectomy patients very high risk for aspiration?

A

they do not have an adequate LES

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77
Q

What is the prevalence of GERD?

A

occurs in 15% of adults

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78
Q

What are the symptoms of GERD?

A

heartburn, regurgitation, dysphagia

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79
Q

What is included in reflux contents?

A

HCL, pepsin, pancreatic enzymes, bile

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80
Q

What are the 3 mechanisms of gastroesophageal incompetence?

A
  1. transient LES relaxation, elicited by gastric distention;
  2. LES hypotension;
  3. Autonomic dysfunction of GE junction
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81
Q

What is normal LES pressure?

A

29 mmHg

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82
Q

What is average GERD LES pressure?

A

13 mmHg

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83
Q

What is the treatment for GERD?

A

avoidance of trigger foods

MEDS: antacids, H2 blockers, PPIs

SURGERY: Nissen fundoplication, Troupet, LINX

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84
Q

What is Nissen fundoplication?

A

treatment of GERD: part of the stomach is wrapped and tracked down around the esophagus like a collar to provide a one-way valve effect

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85
Q

What is a toupet procedure?

A

similar to Nissen procedure but only wrapped halfway around.

86
Q

What is a LINX procedure?

A

It uses titanium magnetic beads to close the LES tighter and when the patient swallows, the force opens the beads and then they close again. ; Mordecai said think of it like a charm bracelet with magnets

87
Q

What medications can we give in preop for GERD patients?

A

cimetidine, ranitidine, PPIs, Sodium citrate, metoclopramide

88
Q

What to cimetadine and ranitidine do pre op to help GI cases?

A

decrease acid secretions and increase pH

89
Q

When do we give PPIs prior to surgery?

A

the night before and morning of surgery

90
Q

What is sodium citrate?

A

PO non-particulate antacid normally given to OB patients prior to C-Section

91
Q

What is the benefit of metoclopramide pre-op?

A

it is gastrokinetic; often reserved for diabetics, obese, and pregnant women

92
Q

What factors increase intra-op aspiration risk? (hella long list)

A

emergency surgery, full stomach, difficult airway, inadequate anesthesia depth, lithotomy, autonomic neuropathy, gastroparesis, DM, pregnancy, increased intrabdominal pressure, severe illnes, morbid obesity

93
Q

How small must particles be to enter into the duodenum?

A

1-2 mm

94
Q

What is the motility of the stomach controlled by?

A

intrinsic and extrinsic neural regulation

95
Q

___________ stimulation to the ____________ nerve increases the number and force of contractions.

A

parasympathetic; vagus

96
Q

__________ stimulation inhibits contractions via the _________ nerve.

A

sympathetic; splanchic

97
Q

The intrinsic nervous system provides ____________ for __________

A

coordination for motility

98
Q

What hormones are involved in neurohormonal control and what is their function?

A

gastrin and motilin increase the strength and frequency of contractions; gastric inhibitory peptide inhibits contractions

99
Q

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

A

peptic ulcer disease

100
Q

What is the prevalence of peptic ulcer disease?

A

lifetime prevalence = 10% women, 12% men; 15,000 deaths per year

101
Q

What bacteria is associated with PUD?

A

Helicobacter pylori

102
Q

What are the symptoms of PUD?

A

burning epigastric pain exacerbated with fasting and improved with meals

103
Q

What is the risk of perforation in PUD if patients do not receive treatment?

A

10% risk of perforation

104
Q

What is the hallmark sign of perforation?

A

sudden/severe epigastric pain caused by acidic secretions into peritoneum

105
Q

What is the cause of death for PUD patients?

A

shock or perforation > 48 hours

106
Q

Whatare acute gastric obstructions caused by?

A

edema and inflammation in pyloric channel at the beginning of duodenum

107
Q

What are symptoms of pyloric obstruction?

A

recurrent vomiting, dehydration, and hyperchloremic alkalosis

108
Q

What are the treatments of pyloric obstruction?

A

NGT, IV hydration; normally resolves in 72 hours

109
Q

What does repetitive ulceration and scarring lead to with gastric obstruction?

A

fixed stenosis and chronic obstruction

110
Q

What are the 5 types of gastric ulcers normally caused by?

A

excessive NSAIDs, H.Pylori, and EtOH

111
Q

What is type 1 gastric ulcer?

A

located along the lesser curvature close to incisura with no acid hyper-secretion

112
Q

What is type 2 gastric ulcer?

A

two ulcers, first on the gastric body, second duodenal, usually with acid hypersecretion

113
Q

What is type 3 gastric ulcer?

A

prepyloric with acid hypersecretion

114
Q

What is type 4 gastric ulcer?

A

at lesser curvature near gastroesophageal junction with no acid hypersecretion

115
Q

What is type 5 gastric ulcer?

A

anywhere in the stomach, usually seen with NSAID use

116
Q

What is Zollinger Ellison Syndrome?

A

Non-B cell islet tumor of the pancreas, causing gastrin hypersecretion

*Gastric acid normally inhibits further gastrin release (neg feedback abscent)

117
Q

What does gastrin do?

A

stimulates gastric acid secretion which normally inhibits further gastrin release (negative feedback loop)

118
Q

What are the symptoms of zollinger ellison syndrome?

A

PUD, erosive esophagitis, diarrhea

119
Q

What is the prevalence of zollinger ellison syndrome?

A

occurs in 0.1-1% of PUD pts; males > females; most commonly between ages 30 and 50; up to 50% of patients with gastrinomas are metastatic at time of diagnosis

120
Q

What is the treatment for zollinger ellison syndrome?

A

PPIs and surgical resection of gastrinoma

121
Q

What are the anesthetic considerations for patients with zollinger ellison syndrome?

A

pts have increased gastric fluid volume, possible electrolytes imbalances, and endocrine abnormalities so: correct electorlytes, increase gastric pH with meds, RSI

122
Q

What happens in the small intestine?

A

small intestinal motility mixes the contents of the stomach with digestive enzymes, further reducing particle size and increasing solubility; Major function of the small intestine is to circulate the contents and expose them to the mucosal wall to maximize absorption of water, nutrients, and vitamins before entering the large intestine

123
Q

What is segmentation?

A

when two nearby areas contract and thereby isolate a segment of intestine. allows the contents to remain in the intestine long enough for the essential substances to be absorbed into the circulation

124
Q

What are reversible causes of small bowel dysmotility?

A

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

125
Q

What are nonreversible structural causes of small bowel dysmotility?

A

scleroderma, connective tissue disorders, IBD

126
Q

What are nonreversible neuropathic causes of small bowel dysmotility?

A

pseudo obstruction in which the intrinsic and extrinsic nervous systems are altered and the intestines can only produce weak, uncoordinated contractions

127
Q

What symptoms does neuropathic small bowel dysmotility lead to?

A

bloating, N/V, abdominal pain

128
Q

What is the function of the large intestine?

A

acts as a reservoir for waste and indigestible material before elimination and it extracts remaining electrolytes and water.

129
Q

What does distention of the ileum do?

A

relaxes the ileocecal valve to allow intestinal contents to enter the colon. subsequent cecal distention will contract the ileocecal valve.

130
Q

What are giant migrating complexes?

A

the produce mass movements across the large intestine and, in the health state, occur approximately 6-10x a day

131
Q

What are the two primary symptoms of colonic dysmotility?

A

altered bowel habits and/or intermittent cramping

132
Q

What are the 2 most common disease associated with colonic dysmotility?

A

IBS (irritable bowel syndrome) and IBD (inflammatory bowel disease)

133
Q

What are the Rome II criteria for IBS?

A

defecation relieves discomfort, pain associated with abnormal frequency (> 3x per day or < 3x per week), pain associated with a change in form of the stool

134
Q

What is required to define IBS?

A

abdominal discomfort alone with 2 of the ROME II criteria

135
Q

What is inflammatory bowel disease?

A

where the contractions are suppressed due to colonic wall compression by the inflamed mucosa but the giant migrating complexes remain and are increased in frequency so their pressure-effect further compresses the inflamed mucosa, which can lead to hemorrhage, thick mucus secretion, and significant erosions.

136
Q

What is the 2nd most common inflammatory disease after rheumatoid arthritis?

A

inflammatory bowel disease

137
Q

What are the two types of IBD?

A

Ulcerative colitis and Crohn’s disease

138
Q

What is the incidence of IBD?

A

18 people in every 100,000

139
Q

What is ulcerative colitis?

A

mucosal disease of rectum in part or all of the colon. in severe cases the mucosa is hemorrhagic, edematous, and ulcerated

140
Q

What are the symptoms of ulcerative colitis?

A

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

141
Q

What labs might be expected for a patient with ulcerative colitis?

A

inc. platelets, inc. erythrocyte sedimentation rate, dec. H&H, dec. albumin

142
Q

What amount of bleeding with ulcerative colitis would warrant surgical colectomy?

A

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

143
Q

What is toxic megacolon?

A

extreme dilation of the colon triggered by electrolyte disturbances

144
Q

What is the mortality rate of colon perforation?

A

15%

145
Q

What is Crohn’s disease?

A

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

146
Q

What is the most common site of inflammation in Crohn’s disease?

A

terminal ilium usually presenting with ileocolitis with RLQ pain and diarrhea

147
Q

What are the 2 patterns of disease with Crohn’s disease?

A

penetrating-fistulas or obstructing

148
Q

What are the symptoms of Crohn’s disease?

A

weight loss, fear of eating, anorexia, diarrhea

149
Q

How does Crohn’s disease progress?

A

persistent inflammation gradually progresses to fibrous narrowing and stricture formation so diarrhea decreases and is replaced by chronic bowel obstruction; extensive inflammation leads to loss of absorptive surfaces resulting in malabsorption and steatorrhea; colonic disease may fistulize into stomach/duodenum causing fecal vomitus

150
Q

What percentage of Crohn’s patients have additional symptoms and what are they?

A

1/3 of patients; symptoms: arthritis, dermatitis, kidney stones

151
Q

What are the medical treatments for IBD?

A

5-acetylsalicylic acid (5-ASA): mainstay for IBD antibacterial and anti-inflammatory; PO/IV glucocorticoids during flares; abx: rifaximin, flagyl, cipro; purine analogues

152
Q

What are the surgical treatments for IBD?

A

last resort and resected segment should be as conservative as possible; small intestine resection should be limited to < 1/2 length; > 2/3 small intestine resection leads to “short bowel syndrome” requiring TPN

153
Q

Where do most carcinoid tumors originate from?

A

the GI tract in any GI tissue/segment

154
Q

What do carcinoid tumors do?

A

secrete peptides and vasoactive substances: gastrin, insulin, somatostatin, motilin, neurotensin, tachykinins, glucagon, serotonin, and other biologic actives

155
Q

What is the occurrence of carcinoid syndrome in patients with carcinoid tumors?

A

10% of patients

156
Q

What is carcinoid syndrome?

A

large amounts of serotonin and vasoactive substances reaching the systemic circulation

157
Q

What are the symptoms of carcinoid syndrome?

A

flushing, diarrhea, HTN/HoTN, bronchoconstriction

158
Q

What heart problems may occur in patients with carcinoid syndrome?

A

pts may acquire right heart endocardial fibrosis; the left heart is generally more protected as the lungs clear some of the vasoactive substances

159
Q

How do we diagnose carcinoid syndrome?

A

urinary or plasma serotonin levels, CT/MRI

160
Q

What is the treatment for carcinoid syndrome?

A

avoid serotonin-triggers, control diarrhea, serotonin antagonists and somatostatin analogues

161
Q

What are our preop considerations for carcinoid syndrome?

A

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

162
Q

What is the incidence of acute pancreatitis?

A

increased 10 fold since the 1960’s likely due to increased alcoholism along with better diagnostics

163
Q

What is autodigestion normally prevented by?

A

proteases packaged in precursor form; protease inhibitors; low intra-pancreatic calcium which decreases trypsin activity

164
Q

What are the two most common causes of acute pancreatitis and how do they cause it?

A

Gallstones and alcohol abuse (60-80% of cases); Gallstones obstruct ampulla of vater causing pancreatic ductal HTN.

165
Q

What are the symptoms of acute pancreatitis?

A

excruciating epigastric pain that radiates to the back, N/V, abdominal distention, steatorrhea, ileus, fever, tachycardia, HoTN

166
Q

What are hallmark labs of acute pancreatitis?

A

increased serum amylase and lipase

167
Q

What imaging might show us acute pancreatitis?

A

contrast CT or MRI, endoscopic US (EUS)

168
Q

What are the complications of acute pancreatitis?

A

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

169
Q

What are the treatments of acute pancreatitis?

A

aggressive IVF, NPO to rest pancreas, enteral feeding (preferred over TPN bc TPN has greater risk of infectious complications), opioids

170
Q

What is the surgical treatment for acute pancreatitis?

A

ERCP (endoscopic retrograde cholangiopancreatography): fluoroscopic examination of biliary and pancreatic ducts; interventions include stone removal, stent placement, sphincterotomy, and hemostasis

171
Q

Is upper or lower GI bleeds more common?

A

upper

172
Q

How much blood loss is necessary in upper GI bleeds to cause HoTN and tachycardia?

A

> 25%

173
Q

What symptom indicate a HCT < 30% with upper GI bleeds?

A

orthostatic HoTN

174
Q

What does melena indicate for upper GI bleeds?

A

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

175
Q

What is BUN level in upper GI bleeds and why?

A

typically > 40 mg/dL due to absorbed nitrogen into bloodstream

176
Q

What is the procedure of choice to diagnose and treat upper GI bleeds?

A

EGD; endoscopic ulcer ligation (perforation risk is 0.5%), ligation of bleeding varices

177
Q

What is the last resort for uncontrolled variceal bleeding?

A

mechanical balloon tampanade

178
Q

What population is most at risk for lower GI bleeds?

A

elderly

179
Q

What are the 3 main causes of lower GI bleed?

A

diverticulosis, tumors, colitis

180
Q

What are the surgical procedures used to treat lower GI bleeding?

A

unprepped sugmoidoscopy performed as soon as the patient is hemodynamically stable; colonoscopy performed if patient can tolerate prep; persistent bleeding warrants angiography and embolic therapy

181
Q

What is an adynamic ileus?

A

colonic ileus characterized by massive dilation of the colon without mechanical obstruction where loss of peristalsis leads to distention of the colon

182
Q

What causes adynamic ileus?

A

may be caused by electrolyte disorders, immobility, excessive narcotics, anticholinergics; may also be due to neural input imbalance of excessive sympathetic stimulation along with inadequate parasympathetic input to the colon

183
Q

What is the treatment for adynamic ileus?

A

restore electrolyte balance, hydrate, mobilize, NG suction, enemas

184
Q

What medication and dose produces immediate results in 80-90% of adynamic ileus patients?

A

neostigmine 2-2.5 mg over 5 minutes; **cardiac monitoring required!!

185
Q

What does adynamic ileus lead to if left untreated?

A

ischemia and perforation

186
Q

How does anxiety in preop affect GI system?

A

higher anxiety = higher inhibition; inhibition of GI activity is directly proportional to the amount of norepi secreted from SNS stimulation

187
Q

How do volatile anesthetics affect the GI system?

A

depress the spontaneous, electrical, contractile, and propulsive activity in the stomach, small intestine, and colon

188
Q

In what order does the GI tract recover from anesthesia?

A

small intestine first, stomach in approx. 24 hours, colon 30-40 hours postop

189
Q

What GI problem is associated with N2O?

A

N2O is 30 x more soluble than nitrogen in the blood and will diffuse into gas-containing cavities so gut distention correlates with the pre-existing amount of gas in the bowel, as well as the duration and concentration of N2O administered.

190
Q

How do NMBDs affect GI motility?

A

they only affect skeletal muscle, GI motility remains intact.

191
Q

How does neostigmine increase PNS activity and bowel peristalsis?

A

by increasing the frequency and intensity of contractions

192
Q

What partially offsets the cholinergic activity of neostigmine?

A

concurrent administration of the anticholinergic medications (glycopyrrolate or atropine) which counteracts the bradycardia associated with neostigmine

193
Q

What effect does sugammadex have on GI motility?

A

none

194
Q

What effect do opioids have on GI motility?

A

reduce GI motility and cause constipation; exert their function on both central and peripheral mu, delta, and kappa receptors

195
Q

What opioid receptors is in the GI system?

A

high density of peripheral mu opioid receptors in the myenteric and submucosal plexuses; Activation of these causes delayed gastric emptying and slower transit through the intestine

196
Q

What adverse GI effects are associated with opioids besides GI motility?

A

nausea, anorexia, delayed digestion, abdominal pain, excessive straining during bowel movements, incomplete evacuation

197
Q

Kahoot

T/F: The liver is the largest internal organ in the human body.

A

True

198
Q

Kahoot

What are the metabolic functions of the liver?
A. carbohydrate metabolism
B. fat metabolism
C. protein metabolism
D. rocuronium metabolism

A

All of the above

199
Q

Kahoot

What part of the liver cleans the blood as it passess through?
A. Space of Disse
B. Hepatocytes
C. Kupffer cells
D. Lymph

A

C. Kupffer cells

200
Q

Kahoot

The liver performs the following:
A. forms many compounds from carbohydrate intermediates
B. glucogenesis
C. conversion of galactose and fructose to glucose
D. storage of large amount of glycogen

A

All of the above

201
Q

Kahoot

The most common cause of cirrhosis is?
A. Biliary obstruction
B. EtOH
C. Chronic viral hepatitis
D. Right sided HF

A

B. EtOh

202
Q

Kahoot

T/F: Cirrhosis results in splenomegaly, esophageal varices, and left heart failure.

A

False

203
Q

Kahoot

Cirrhotic patients should be resuscitated with:
A. colloids
B. crystalloids

A

A. Colloids

204
Q

Kahoot

Vitamin K is used to treat an elevated PT which measures which coagulation pathway?
A. intrinsic
B. extrinsic

A

B. extrinsic

205
Q

Kahoot:

A platelet count less than —– required preop replacement.
A. 100 K
B. 150 K
C. 50 K
D. 75 K

A

C. 50K

206
Q

Kahoot

T/F: Chronic alcoholism increases MAC for isoflurane and this is probably due to cross-tolerance.

A

True

207
Q

Kahoot

T/F: Anesthetic drugs may cause post-op liver dysfunction to be exaggerated.

A

True

208
Q

Kahoot

Plasma cholinesterase may be —– in severe liver disease.
A. Increased
B. Decreased

A

B. Decreased

209
Q

Kahoot:

Manifestations of alcohol withdrawal occur in —– hours after no alcohol intake.
A. 24-72 hrs
B. 4-8 hrs
C. 6-12 hrs
D. 12-24 hrs

A

A. 24-72 hours

210
Q

Kahoot

T/F: Hepatitis A is the most commonly transmitted blood-bourne pathogen.

A

False

211
Q

Kahoot:

Drugs that cause hepatitis include:
A. analgesics
B. anticonvulsants
C. VAAs
D. tranquilizers

Is VAAs volatiles?

A

All of the above

212
Q

Kahoot

What surgical procedure is associated with the highest mortality?
A. BKA
B. laparotomy
C. ORIF of the tibia
D. coronary angioplasty

A

B. laparotomy

Health Assessment (8 decks)

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