GI Diseases (Exam IV)-Mordekai Flashcards

1
Q

How much of the total body mass does the GI tract constitute?

A

5%

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2
Q

What are the 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 the outermost to the innermost?

A
  • Serosa
  • Longitudinal muscle layer
  • Circular muscular layer
  • Submucoas
  • Mucosa
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4
Q

What are the layers of the mucosa from the outermost to innermost?

A
  • Muscularis mucosae
  • Lamina propria
  • Epithelium
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5
Q

What is the serosa layer of the GI system?

A

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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6
Q

What is the longitudinal muscle layer of the GI system?

A

This layer contracts to shorten the length of the intestinal segment.

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7
Q

What is the circular muscle layer of the GI system?

A

This layer contracts to decrease the diamter of the intestinal lumen.

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8
Q

What 2 GI layers work together to propogate gut motility?

A
  • Longitudinal muscle layer
  • Circular muscle layer
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9
Q

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

A

The celiac plexus

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10
Q

What innervates the descending colon and distal GI tract?

A

The inferior hypogastric plexus

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11
Q

What 4 approaches can block the celiac plexus?

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

Where is the myenteric plexus located?

A
  1. Lies between the smooth muscle layers and regulates the smooth muscle.
    * Located in the muscularis layer
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13
Q

Where is the submucosal plexus located?

A
  • Transmits information from the epithelium to the enteric and central nervous system
  • Located in the submucosa layer
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14
Q

What is the mucosa layer of the GI tract composed of?

A
  • A thin layer of smooth muscle called the muscularis mucosa, which functions to move the villi.
  • The lamina propria, chich contains blood vessels and nerve endings.
  • Immune and inflammatory cells
  • The epithelium, Where the GI contents are sensed, enzymes are secreted, nutrients are absorbed, and waste is excreted.
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15
Q

What innervates the GI tract?

A

Autonomic nervius system

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16
Q

What does the GI ANS consist of?

A
  • The oextrinsic nervous system - Has SNS and PNS components. SNS is primarily inhibitory and decreases GI motility. PNS is primarily excitatory and activates GI motility.
  • Enteric nervous system - This is the independent nervous system that controls motility, secretion, and blood flow.
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17
Q

What does the myenteric plus control?

A

Motility which is carried out by enteri neurons, interstitial cells of cajal (ICC. GI pacemaker), and smooth muscle cells.

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18
Q

What 3 things does the submucosal plexus control?

A
  • Absorption
  • Secretion
  • and mucosal blood flow
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19
Q

True/False
The myenteric and submucosal plexus respond to sympathic and para sympathetic stimulation,

A

true

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20
Q

What is an upper gastrointestinal endoscopy?

A
  • May be diagnostic or therapeutoc endoscope placed into the esophagus, stomahc, pylorus, and duodenum.
  • May be done with ot out anesthesia
  • Anesthesia challenges = sharing airway with endoscopist
  • Procedure is typically performed outside the main OR.
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21
Q

What is a colonoscopy?

A
  • May be diagnostic, therapeutic or interventional
  • May be done with or without anesthesia
  • Anesthesia challenges = patient dehydration due to bowel prep and NPO status.
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22
Q

What is a high resolution manometry (HRM)?

A
  • A pressure catheter that measures pressure along the entire esophageal length.
  • Generally used to diagnose motility disorders
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23
Q

What is a GI series with ingested barium test?

A

A radiologic assessment of swallowing function and GI transit

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24
Q

What is a gastric emptying study?

A

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

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25
Q

What is a small intestine manometry?

A
  • A catheter that measures contraction pressures and motility of the small intestine.
  • Evaluates contractions during 3 periods: fasting, during a meal, and post-prandial.
  • Normally the recording time consists of 4 hours fasting, followed by ingestion of a meal, and then 2-hours post meal.
  • Abnormal results are grouped into myopathic and/or neuropathic causes
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26
Q

What is a lower GI series test?

A
  • Involves the administration of a barium enema to the patient.
  • The barium outlines the intestines and it is visible on radiograph.
  • This allows for detection of colon and rectal abnormalities.
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27
Q
  • What is an esophageal disease?
  • What are the 3 different groups?
A
  • Diseases of the esophagus
  • Groups = anatomical. mechanical, and neurologic.
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28
Q

What are anatomical causes of esophageal diseases?

A
  • diverticula
  • hiatal hernia
  • changes associated with chronic acid reflux.
  • These abnormalities interupt the normal pathway of food, which changes the pressure zones of the esophagus.
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29
Q

What are the mechanical causes of esophageal diseases?

A
  • Achalasia
  • esophageal spasms
  • hypertensive LES
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30
Q

What are the neurologic causes of esophageal diseases?

A
  • May be caused by neurologic disorders such as a stroke, vagotomy, or hormone deficiencies.
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31
Q

What are general symptoms of esophageal diseases?

A
  • Dysphagia
  • Heartburn
  • GERD
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32
Q
  • What is dysphagia?
  • Differentiate the 2 types.
A
  • Difficulty swallowing, may be oropharyngeal or esophageal
  • Oropharyngeal dysphagia = common after head and neck surgeries.
  • Esophageal dysphagia = classified based on physiology. Esophageal dysmotility symptoms occur with both liquids and solids. Mechanical esophageal dysphagia symptoms occur only with solid food.
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33
Q
  • What is GERD?
  • What are the symptoms?
A
  • Gastroesophageal reflux disease
  • An effortless return of gastric contents into the pharynx
  • Symptoms include heartburn, nausea, and lump in the throat feeling.
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34
Q

What is achalasia?
What does it cause?

A
  • A neuromuscular disorder of the esophagus consisting of an outflow obstruction due to inadequate LES tone and a dilated hypomobile esophagus.
  • Reduced peristalsis and dilated espophagus
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35
Q

What is achalasia caused by?

A
  • Theoretically caused by loss of ganglionic cells of the esophageal myenteric plexus.
  • Followed by absence of inhibitory neurotransmitters of the LES.
  • Unopposed cholinergic LES stimulation (LES can’t relax)
  • Esophageal dilation with food unable to pass into the stomach.
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36
Q
  • What are the symptoms of achalasia?
  • What is achalasia a long term increased risk of?
A
  • S/S = dysphagia, regurgitation, heartburn, and chest pain.
  • Long term increased risk for esophageal cancer
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37
Q

How is achalasia diagnosed?

A

Diagnosis made with esophageal manomertry and or esophpgram.

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38
Q

What is a type 1 achalasia class?

A
  • Minimal esophageal pressure
  • responds well to myotomy
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39
Q

What is a type 2 achalasia class?

A
  • Entire esophagus pressurized
  • Responds well to treatment
  • Has the best outcomes
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40
Q

What is a type 3 achalasia class?

A
  • Esophageal spasms with premature contractions
  • Has the worst outcomes
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41
Q

What are the treatments for achalasia?

A
  • All treatments are palliative.
  • Medications = nitrates and CCBs to relax LES
  • Endoscopic botox injections
  • Pneumatic dilation (most effective nonsurgical treatment)
  • Laparoscopic hellar myotomy (best surgical treatment)
  • POEM - peri-oral endoscopic myotomy. Endoscopic division of LES muscle layers. (40% develop pneumothorax or pneumoperitoneum).
  • Esophagectomy - only considered in the most advanced disease states.
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42
Q

What are achalasia patients at risk for and what type of intibation is indicated?

A
  • Increased risk for aspiration.
  • Needs RSI or awake intubation
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43
Q

Differentiate dysphagia and odynophagia.

A
  • Dysphagia - difficulty swallowing
  • Odynophagia - painful swallowing
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44
Q

What is a normal LES (lower esophageal sphincter) resting tone?

A

29 mmHg

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45
Q

What is the biggest risk with achalasia?
How would anesthetic practices change for a achalasia patient?

A
  • Aspiration
  • NPO for 24-48 hours prior to Heller myotomy or POEM.
46
Q

How would a esophageal motility vs structural issue be delineated?

A
  • Structural = difficulty w/ solids
  • Motility = difficulty w/ solids & liquids.
47
Q
  • What is a diffuse esophageal spasm?
  • What population is it more common in?
  • How is it diagnosed?
  • What are the S/S?
A
  • A spasm that usually occurs in the distal esophagus likely due to autonomic dysfunction,
  • More common in the elderly
  • Diagnosed with an esophram
  • S/S - pain mimics angina
48
Q

What would an esophageal spasm look like under direct visualization?

A
  • Corkscrew or rosary bead appearance.
49
Q

What medications could be used to treat esophageal spasms?

A
  • Nitroglycerin
  • Trazodone
  • Imipramine
  • Sildenafil
  • Antidepressants
  • PD-I’s
50
Q

What is an esophageal diverticulum?
What kinds are there?

A

Esophageal wall out-pouching
- Pharyngoesophageal (Zenker’s)
- Mid-esophageal
- Epiphrenic (supradiaphragmic)

51
Q

What are the main symptoms of esophageal diverticula?

A
  • Halitosis (bad breath)
  • Dysphagia (worse with larger pockets)
52
Q

What is the treatment for esophageal diverticula?

A
  • Small - medium: nothing
  • Medium - large: removal
53
Q

What are anesthesia considerations and risks for esophageal diverticula?

A
  • No cricoid pressure
  • Avoid NGT
  • Intubate w/ head elevated
  • Aspiration risk
54
Q

What type of hernia is depicted by 1 on the figure below?

A

Normal (no hernia)

55
Q

What type of hernia is depicted by 2 on the figure below?

A

Sliding Hiatal hernia

56
Q

What type of hernia is depicted by 3 on the figure below?

A

Paraesophageal Hiatal hernia

57
Q

What types of cancer are normally seen with esophageal cancer?
Where are they located typically?

A
  • Squamous cell carcinoma (mid-esophagus)
  • Adenocarcinomas (distal esophagus)
58
Q

What signs/symptoms are indicative of esophageal cancer?

A
  • Progressive dysphagia
  • Weight loss
  • Pancytopenia
  • Lung Injury
  • Malnourishment/dehydration
59
Q

What is the treatment for esophageal cancer?

A
  • Esophagectomy
  • Chemotherapy
  • Radiation
60
Q

What deficient LES pressure is typically seen with GERD?

61
Q

What typically causes GERD?

A
  • LES hypotension
  • GE junction abnormality (hiatal hernia)
62
Q

What complications can occur with chronic GERD?

A
  • Esophagitis
  • Laryngopharyngeal reflux
  • Recurrent pulmonary aspiration (chronic cough)
63
Q

What treatments are used for GERD?

A
  • Lifestyle modifications
  • PPIs > H2 antagonists
  • Niessen fundiplocation
64
Q

What are anesthesia considerations for GERD patients?

A

Manage Aspiration risk

  • Ranitidine > cimetidine
  • PPI’s
  • Na⁺ citrate + reglan
  • RSI + Cricoid pressure recommended.
65
Q

What is peptic ulcer disease (PUD) ?
How does it present and what causes it?

A
  • Ulcers of mucosal lining of stomach or duodenum causing a burning epigastric pain; caused by H. Pylori decreasing normal gastric mucosa HCO₃⁻ .
  • H. Pylori + NSAIDs.
66
Q

Who is at greater risk for PUD?

A
  • Alcoholics
  • Elderly
  • Malnourished
67
Q

What significant risk factors come from untreated PUD?

A
  • Bleeding
  • Peritonitis → sepsis
  • Dehydration
  • Perforation
68
Q

What is the mortality risk of bleeding from PUD?

69
Q

What sort of perforation risk is conferred from untreated PUD?
What symptom is seen with perforation?

A
  • 10% risk
  • Sudden and severe epigastric pain
70
Q

What drugs (along with abbreviated MOA’s) are used to treat PUD?

A
  • Antacids (OTC relief of dyspepsia)
  • H2 receptor antagonists (ranitidine & famotidine are better than cimetidine)
  • PPI’s
  • Prostaglandin Analogues (Misoprostol maintains mucosal integrity)
  • Cytoprotective agents (Sucralfate creates chemical barrier)
71
Q

How is H. Pylori treated?

A
  • PPI + 2 ABX for 14 days
72
Q

Which antibiotics are used for H. Pylori treatment?

A
  • Clarithromycin and amoxicillin or metronidazole.
73
Q

What is post-gastrectomy dumping syndrome?

A
  • Release of GI vasoactive hormones from pyloric sphincter dysfunction causing food to move from the stomach into small bowel too early.
74
Q

Differentiate Early vs Late Dumping syndrome.

A
  • Early - lots of symptoms (cramping, ↓BP, N/V/D, etc)
  • Late - Hypoglycemia
75
Q

What is the treatment for dumping syndrome?

A
  • Dietary modifications
  • Octreotide
76
Q

What is ulcerative colitis?
What are all the signs/symptoms?

A
  • Mucosal disease involving all or most of the colon to rectum.
  • Bleeding, tenesmus, N/V/D, fever, and weight loss.
77
Q

What is tenesmus?

A
  • Tenesmus = Urge to poop
78
Q

What major complications can occur with severe ulcerative colitis ?

A
  • Massive hemmorrhage
  • Toxic megacolon
  • Obstruction
  • Perforation
79
Q

What is the surgical treatment for ulcerative colitis?

A
  • Total proctocolectomy
80
Q

What is Crohn’s disease?
What are the symptoms?

A
  • Acute/Chronic bowel inflammation
  • Weight loss, inflammatory mass, bowel spasm, steatorrhea, & stricture formation.
81
Q

What anatomical feature separates the small and large intestine?

A

Ileocecal valve

82
Q

What surgical treatment exists for severe Crohn’s disease?

A
  • Bowel resection
  • Proctocolectomy
83
Q

What medical treatment exists for mild-moderate IBS?
What meds are used in severe cases?

A
  • Normal cases: 5-ASA, glucocorticoids, ciprofloxacin and metronidazole.
  • Severe cases: Azathioprine & 6MP or methotrexate & cyclosporine
84
Q

What organs are a part of the foregut?

A
  • Thymus
  • Esophagus
  • Lungs
  • Stomach
  • Duodenum
  • Pancreas
85
Q

What organs are a part of the midgut?

A
  • Appendix
  • Ileum
  • Cecum
  • Ascending Colon
86
Q

What organs are a part of the hindgut?

A
  • Distal large intestine
  • Rectum
87
Q

Less than _____% of carcinoid tumors originate in the lung tissue.
What “gut” are the lungs located in?

A
  • 25%
  • Foregut
88
Q

What do carcinoid tumors secrete?

A
  • Insulin
  • Histamine
  • Serotonin

GI peptides and/or vasoactive substances

89
Q

Compare/contrast serotonin secretion from all parts of the gut.

A
  • Foregut - Low serotonin secretion
  • Midgut - High serotonin secretion
  • Hindgut - Rare serotonin secretion
90
Q

Which part of the gut is prone to development of carcinoid syndrome?

A
  • Midgut

Foregut is atypical, hindgut is rare.

91
Q

What is carcinoid crisis/syndrome?
What are the signs & symptoms?

A
  • Release of serotonin and/or histamine from carcinoid tumor.
  • Flushing, diarrhea, ↓↑BP, bronchostriction/wheezing.
92
Q

What symptoms commonly present with small intestine carcinoid tumor?

A
  • Abdominal pain (51%)
  • Intestinal obstruction (31%)
93
Q

What symptoms commonly present with rectal carcinoid tumors?

A
  • Bleeding (39%)
94
Q

What symptoms commonly present with bronchus carcinoid tumors?

A
  • Asymptomatic (31%)
95
Q

Where are metastases from carcinoid tumors most often found?
What is the presenting symptom?

A
  • Liver; found via hepatomegaly
96
Q

What most often provokes carcinoid crisis?

A
  • Biopsy of tumor
  • Chemo
  • Stress
97
Q

What drugs may provoke mediator release (serotonin, histamine, etc) from carcinoid tumors?

A
  • Succinylcholine
  • Atracurium
  • Epi/NE
  • Dopamine
  • Isoproterenol
  • Thiopental
98
Q

What drugs are used in the treatment of carcinoid tumor crisis?

A
  • 5HT blockers
  • H-antagonists
  • Somatostatin analogues (Octreotide)
  • Ipratropium
99
Q

How do somatostatin analogues treat carcinoid tumor patients?

A
  • Prevention of Carcinoid Crisis
100
Q

What are the causes of acute pancreatitis?

A
  • Gallstones & EtOH abuse (60-80% of cases)
  • AIDS
  • Hyperparathyroidism
  • Trauma
101
Q

What lab values indicate acute pancreatitis?

A
  • ↑ serum amylase & lipase
102
Q

What do the Ranson criteria indicate?
What would the below indicate:
- 0-2 criteria?
- 3-4 criteria?
- 5-6 criteria?
- 7-8 criteria?

A
  • Ranson Criteria indicate severity & mortality of acute pancreatitis.
  • 0-2 = <5% mortality
  • 3-4 = 20% mortality
  • 5-6 = 40% mortality
  • 7-8 ≈ 100% mortality
103
Q

What are treatments for acute pancreatitis?

A
  • Aggressive IV fluids
  • Colloids
  • NPO
  • Enteral/TPN
  • NGT suction
  • Pain management
  • Gallstone removal
104
Q

What are signs/symptoms of chronic pancreatitis?

A
  • Post-prandial epigastric pain
  • Emaciated
  • Steatorrhea
  • DM
105
Q

What conditions put one at risk of chronic pancreatitis?

A
  • Chronic EtOH
  • Cystic fibrosis (?)
  • Hyperparathyroidism
106
Q

What’s the number one cause of upper gastric GI bleeding? Number 2?

A
  1. Varices
  2. Peptic Ulcer Disease
107
Q

Where are bleeding uclers most often found in peptic ulcer disease?

A
  • Duodenal (36%)
  • Gastric (24%)
108
Q

What is the most common cause of lower GI bleeding?

A
  • Colonic Diverticulosis (41%)
109
Q

What characterizes initial acute upper GI bleeding?

A
  • ↓BP and ↑HR w/ 25% or more blood loss
  • HCT normal at beginning
  • Anemia
110
Q

What are signs of chronic upper GI bleeding?

A
  • Orthostatic hypotension from Hct <30%
  • BUN >40mg/dL
111
Q

What anesthetic technique should be employed for upper GI bleeding?

A
  • RSI (rapid sequence intubation)
112
Q

In patients with carcinoid tumors, how early should octreotide be administered to prevent crisis during surgery:

A. 4 hours
B. 24 hours
C. 12 hours
D. 8 hours

A

B. 24 hours