Exam 4 - Gastrointestinal Assessment Flashcards

1
Q

The GI system constitutes ____ of the body mass

A

5%

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2
Q

The main functions of the GI system include:

A

motility, digestion, absorption, excretion, and circulation

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3
Q

From outermost to innermost, the GI layers are:

A

serosa, longitudinal muscle layer, circular muscle layer, submucosa, and mucosa

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4
Q

Within the mucosa, the outermost to innermost layers are:

A

muscularis mucosae, lamina propria, and epithelium

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5
Q

What is the function of the muscularis mucosa?

A

Move the villi

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6
Q

What is contained within the lamina propria?

A

Contains blood vessels, nerve endings, and immune cells

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7
Q

What happens within the epithelium of the mucosa?

A
  • GI contents are sensed
  • Enzymes are secreted
  • Nutrients are absorbed
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8
Q

What is the purpose of the longitudinal muscle layer?
The circular muscle layer?

A
  • Longitudinal muscle layer - contracts to shorten the length of the intestinal segment
  • Circular muscle layer - contracts to decrease the diameter of the intestinal lumen
  • Both layers work together to promote motility
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9
Q

This innervates the proximal GI organs to the transverse colon?

A

Celiac plexus

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10
Q

What innervates the descending colon and distal GI tract?

A

Hypogastric plexus

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10
Q

How can the celiac plexus be blocked?

A
  • Trans-crural
  • Intraoperative
  • Endoscopic ultrasound-guided
  • Peritoneallavage
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11
Q

What nerve lies between the smooth muscles layers of the intestines?

A

Myenteric plexus

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12
Q

What nerve transmits information from the epithelium to the eneteric and central nervous system?

A

Submucosal plexus

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13
Q

The GI tract is innervated by the ____ , which consists of the ____ and ____

A
  • ANS
  • Extrinsic nervous system
  • Enteric nervous system
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14
Q

What are the components of the extrinsic nervous system?

A

SNS and PNS components
* The extrinsic SNS is primarily inhibitory anddecreases GI motility
* The extrinsic PNS is primarily excitatory and activates GI motility

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15
Q

The enteric nervous system is the ____ nervous system and includes ____ and ____ innervations

A
  • Independent
  • Myenteric
  • Submucosal
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16
Q

What does the myenteric plexus control?

A

Motility via enteric neurons, interstitial cells of Cajal (ICC cells, pacemaker cells), and smooth muscle cells

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17
Q

The submucosal layer controls:

A

Absorption, secretion, and mucosal blood flow

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18
Q

The myenteric and submucosal plexus respond to what stimulation?

A

Both PNS and SNS

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19
Q

What are the anesthesia challenges with an EGD?

A
  • Sharing airway with endoscopist
  • Usually done without ETT, must closely manage airway
  • Procedure performed outside of the main OR (limited equipment & supplies)
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20
Q

Anesthesia challenges for a colonoscopy?

A

Pt is dehydrated d/t bowel prep and NPO status

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21
Q

What test uses a pressure catheter to diagnose motility disorders?

A

High Resolution Manometry (HRM)

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22
Q

What test is used to assess swallowing function radiologically?

A

Barium GI series

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23
Q

How does a gastric emptying study work?

A

Pt fasts for 4 hours, then consumes a meal with a radiotracer - then completes frequent imaging withing the next 1-2 hours

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24
Q

What does the small intestine manometry test evaluate?
How are abnormal results grouped?

A
  • Evaluatescontractions during three periods: fasting, during a meal, and post-prandial
  • Myopathic and or neuropathic
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25
Q

What test allows for radiographic evaluation of the colon/rectum with the use of barium?

A

Lower GI series

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26
Q

What are the anatomical esophageal diseases?

A
  • diverticula
  • hiatal hernia
  • changes assoc w/ chronic acid reflux
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27
Q

What are the mechanical esophageal diseases?

A
  • achalasia
  • esophageal spasms
  • hypertensive LES
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28
Q

What are the neurological esophageal diseases?

A
  • stroke
  • vagotomy
  • hormone deficiencies
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29
Q

What are the most common symptoms of espohageal disease?

A
  • Dysphagia
  • Heartburn
  • GERD
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30
Q

What are esophageal dysmotility and mechanical esophageal dysphasia?

A
  • Esophageal dysmotility: sx occur w/ both liquids & solids
  • Mechanical esophageal dysphasia: sx only occur w/solid food
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31
Q

What is achalasia?

A

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

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32
Q

What is the patho of achalasia?

A
  • Theoretically, c/b loss of ganglionic cells of the esophageal myenteric plexus
  • Followed by absence of LES inhibitory neurotransmitters
  • Unopposed cholinergic LES stimulation (LES can’t relax)
  • Esophageal dilation with food unable to move forward
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33
Q

Symptoms of achalasia?

A

dysphagia, regurgitation, heartburn, chest pain

34
Q

What is long-term achalasia associated with?
What are the 3 classes?

A
  • Increased risk of esophageal cancer
  • Type 1: minimal esophageal pressure, responds well to myotomy
  • Type 2: entire esophagus pressurized; responds well to treatment, has best outcomes
  • Type 3: esophageal spasms w/premature contractions; has worst outcomes
35
Q

Treatments for achalasia?
Which one is most effective surgical and nonsurgical option?

A

All treatments are palliative, not curative
- CCB and nitrates to relax LES
- Endoscopic botox
- Pneumatic dilation - most effective non surgical
- Laproscopic Hellar Myotomy - most effective surgical
- Perioral endoscopic myotomy (POEM) - division of muscle layers, high risk of pneumo
- Esophagectomy - last option

36
Q

What esophageal disorder can mimic angina?
Treatments?

A

Esophageal spasms
Tx: NTG, antidepressants, PDI’s

37
Q

What is an esophageal diverticula and the different types?

A

Outpouchings in the wall of the esophagus
Pharyngoesophageal (Zenker diverticulum): bad breath d/t food retention
Midesophageal: may be caused by old adhesions or inflamed lymph nodes
Epiphrenic (supradiaphragmatic): pts may experience achalasia

38
Q

What disorder is caused by weakend connective tissues that anchor the GE junction to the diaphragm?

A

Hiatal hernia

39
Q

What are the primary and secondary types of esophageal cancers?

A
  1. Adenocarcinomas
  2. Squamos Cell carinoma
40
Q

What procedure carries a high risk of recurrent laryngeal nerve injury?
Anesthesia concerns?

A

Esophagectomy
- Malnutrition
- Chemo/radiation = pancytopenia and dehydration

41
Q

Contents of reflux?

A
  • HCL
  • pepsin
  • pancreatic enzymes
  • bile
42
Q

Bile reflux is associated with ?

A
  • Barrest metaplasia
  • Adneocarinoma
43
Q

What are the 3 mechanisms of GE incompetence?

A
  • Transient LES relaxation, elicited by gastric distention
  • LES hypotension (normal LES pressure 29mmHg, avg GERD pressure 13 mmHg)
  • Autonomic dysfunction of GE junction
44
Q

Treatments for GERD?

A
  • avoidance of trigger foods
  • Meds: Antacids, H2 blockers, PPIs
  • Surgery: Nissen Fundoplication, Toupet, LINX
45
Q

Preop medications for pts with GERD?

A
  • Cimetidine, Ranitidine- ↓acid secretion & ↑ gastric pH
  • PPI’s generally given night before and morning of
  • Sodium Citrate- PO nonparticulate antacid
  • Metoclopramide- gastrokinetic; often reserved for diabetics, obese, pregnant
46
Q

How does PNS and SNS stimulation effects the stomach?

A
  • PNS stimulates the vagus nerve to increase the number and force of contractions
  • SNS stimulation to the splanchnic nerve inhibits these contractions
47
Q

What are the neurohormonal controls over GI movement?

A
  • gastrin & motilin increase the strength and frequency of contractions
  • gastric inhibitory peptide inhibits contractions
48
Q

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

A

Peptic Ulcer Disease

49
Q

Symptoms of PUD?
Major adverse effect?

A
  • Burning epigastric pain exacerbated w/fasting and improved w/meals
  • Perforation
50
Q

What bacteria is associated with PUD?

A

Helicobacter Pylori

51
Q

Symptoms and treatments for gastric outlet obstruction?

A
  • Sx: Recurrent vomiting, dehydration & hyperchloremic alkalosis
  • Tx: NGT, IV hydration; Normally resolves in 72h
52
Q

Types of gastric ulcers?

53
Q

H. pylori treatment?

A

Tripple therapy (2abx+ PPI) x 14 days

54
Q

What is Zollinger Ellison syndrome?

A

Non B cell pancreatic tumor (gastrinoma), causing gastrin hypersecretion
Gastrin stimulates gastric acid secretion. Gastric acid normally inhibits further gastrin release (neg feedback)
This feedback loop is absent in ZE syndrome

More common in men than women

55
Q

Common abnormalities with ZE syndrome?
Treatments?

A

Pts have ↑ gastric volume, e-lyte imbalances, & endocrine abnormalities
Tx: PPIs and surgical resection of gastrinoma

56
Q

Major function of the small intestines?

A

Circulate contents and expose them to the mucosal wall to maximize absorption

57
Q

What is segmentation?
What controls it?

A
  • When two nearby areas contract and isolate a segment to hold the contents in place long enough to be absorbed into the circulation
  • Controlled mainly by the enteric nervous system with motility controlled by the extrinsic nervous system
58
Q

What are the 2 classes of nonreversible small bowel dysmotility?
What disorders are included in each?

A

Structural: scleroderma, connective tissue disorders, IBD
Neuropathic:pseudo-obstruction

59
Q

Where are giant migrating complexes found? What is their function?

A
  • The colon
  • Giant migrating complexes serve to produce mass movements across the large intestine
  • In the healthy state, these complexes occur approximately 6-10x a day
60
Q

How does colonic dysmotility present?

A

Altered bowel habits and or intermittent cramping

61
Q

Patho of IBD?
What is included in IBD?

A
  • contractions are suppressed due to inflammation, but the giant migrating complexes remain
  • The increased frequency of giant migrating complexes further compresses the inflamed mucosa, which can lead to significant erosions and hemorrhage
  • Includes Chrones and UC
62
Q

What are the1st and 2nd most common inflammatory diseases?

A
  1. Rheumatoid arthritis
  2. IBD
63
Q

What is Ulcerative Colitis?
Symptoms?
Lab findings?

A
  • Mucosal disease of part of all of the colon
  • Causes diarrhea, rectal bleeding, crampy abdominal pain, N/V, fever, weight loss
  • Labs: may have ↑plts,↑erythrocyte sedimentation rate,↓H&H,↓albumin
64
Q

When do UC patients require surgery?

A
  • Hemmorhage requiring 6 or more units in 24 hours
  • Toxic megacolon
65
Q

Patho of Chron’s disease?

A
  • Acute or chronic inflammatory process that may affect any/all of the bowel
  • Most common site is the terminal ileum
  • Inflammation causes fibrous narrowing and strictures → chronic bowel obstruction
66
Q

What additional symptoms may Chron’s patients have?

A
  • Arthritis
  • Dermatitis
  • Kidney stones
67
Q

Medical treatments for IBD?

A
  • 5-Acetylsalicylic acid (5-ASA)- mainstay for IBD antibacterial & anti-inflammatory
  • PO/IV Glucorticoids during flares
  • Antibiotics: Rifaximin, Flagyl, Cipro
  • Purine analogues
68
Q

Surgical considerations for IBD?

A
  • Should be last resort
  • Should not resect more than 2/3 of the small intestine to prevent short bowel syndrome
69
Q

Where do most carcinoid tumors originate?
What do they secrete?

A

From the GI tract in any area
Secretes peptides and vasoactive substances

70
Q

What is carcinoid syndrome?
Symptoms?

A
  • Lg amts of serotonin & vasoactive substances reach systemic circulation
  • Sx: flushing, diarrhea, HTN/HoTN, bronchoconstriction, right heart endocardial fibrosis
71
Q

Tx and preop conerns for carcinoid tumors?

A

Tx: avoid serotonin-triggers, serotonin antagonists & somatostatin analogues
Preop: Octreotide before surgery and prior to tumor manipulation to attenuate volatile hemodynamic changes

72
Q

Why has pancreatitis increased since 1960s?

A

Increased alcholism and better diagnostics

73
Q

How is normal autodigesteion prevented in the pancreas?

A
  • Proteases packaged in precursor form
  • Protease inhibitors
  • Low intra-pancreatic calcium, which decreases trypsin activity
74
Q

Common causes of pancreatitis?

A
  • Gallstones
  • EtOH
  • Immunodeficency syndrome → Hyperparathyroidism (increased Ca++)
75
Q

Hallmark labs in pancreatitis?

A

↑serum amylase & lipase

76
Q

Serious complications of pancreatitis?
Treatments?

A

Complications: shock, ARDS, renal failure, necrotic pancreatic abscess
Tx: Aggressive IVF, NPO to rest pancreas, enteral feeding (preferred over TPN), opioids, ERCP
TPN associated w/greater risk of infectious complications

77
Q

____ blood loss will lead to HoTN & tachycardia
Orthostatic HoTN normally indicates HCT ____
____ indicates bleed is above the cecum (where SI meets colon)

A

> 25% blood loss will lead to HoTN & tachycardia
Orthostatic HoTN normally indicates HCT < 30%
Melena indicates bleed is above the cecum (where SI meets colon)

78
Q

Why is BUN elevated in GI bleeding?

A

Typically > 40 d/t absorbed nitrogen into bloodstream

79
Q

Ileus treatments?

A

Restore e-lyte balance, hydrate, mobilize, NG suction, enemas
Neostigmine 2-2.5mg over 5 min

80
Q

What can cause GI inhbition related to surgery?

A

Preop anxiety - increased SNS stimulation
Volatile anesthetics - depresses electrical, contractile, and propulsive GI activity

81
Q

How does the GI tract recover from anesthesia?

A

small intestine → stomach (24 h) → colon (30-40h)

82
Q

What should be avoided in lengthy abdominal surgeries?

83
Q

What receptors cause delayed gastric emptying from opioids?

A

Mu receptors