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Health Assessment Exam 4 > GI- (Exam IV, Mordecai) > Flashcards

GI- (Exam IV, Mordecai) Flashcards

1
Q

What are the 5 main functions of the GI tract?

A

Motility, digestion, absorption, excretion, and circulation.

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2
Q

What are the layers of the GI wall (outer to inner)?

A

Serosa → Longitudinal muscle → Circular muscle → Submucosa → Mucosa.

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3
Q

What are the layers within the mucosa?

A

Muscularis mucosae → Lamina propria → Epithelium.

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4
Q

What do the longitudinal and circular muscle layers do?

A

Longitudinal: Shortens the intestine.
Circular: Narrows the lumen.

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5
Q

What is the role of the epithelium in the GI tract?

A

Senses contents, secretes enzymes, absorbs nutrients.

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6
Q

How is the GI tract innervated?

A

Extrinsic ANS:
SNS: Inhibits motility
PNS: Stimulates motility
Enteric system: Controls motility, secretion, and blood flow.

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7
Q

What are the two plexuses of the enteric nervous system?

A

Myenteric (Auerbach’s): Controls motility
Submucosal (Meissner’s): Controls secretion, absorption, mucosal blood flow.

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8
Q

What are the interstitial cells of Cajal (ICC)?

A

GI pacemaker cells located in the myenteric plexus.

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9
Q

What does the celiac plexus innervate?

A

Proximal GI organs to the transverse colon.

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10
Q

What does the hypogastric plexus innervate?

A

Descending colon and distal GI tract.

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11
Q

What areas are examined in an upper GI endoscopy?

A

Esophagus, stomach, pylorus, and duodenum.

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12
Q

What are anesthesia concerns during upper GI endoscopy?

A

Airway shared with endoscopist, typically no ETT, done outside OR with limited resources.

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13
Q

What is the main concern during colonoscopy anesthesia?

A

Dehydration due to bowel prep and NPO status.

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14
Q

What does high-resolution manometry (HRM) assess?

A

Esophageal pressure and motility.

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15
Q

What is a gastric emptying study?

A

Patient eats a radiolabeled meal → serial imaging over 1–2 hrs to assess gastric motility.

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16
Q

What does small intestine manometry measure?

A

Contraction pressures during fasting, feeding, and post-prandial periods.

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17
Q

What is a lower GI series?

A

Barium enema + X-ray to detect colon/rectal abnormalities.

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18
Q

What are the 3 main categories of esophageal disease?

A

Anatomical, mechanical, neurologic.

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19
Q

How does esophageal dysphagia differ from oropharyngeal dysphagia?

A

Esophageal: Food gets stuck after swallowing
Oropharyngeal: Difficulty initiating swallow, often post-head/neck surgery.

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20
Q

What are the 2 types of esophageal dysphagia?

A

Esophageal dysmotility: Symptoms with solids and liquids
Mechanical dysphagia: Symptoms with solids only.

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21
Q

What is achalasia?

A

Neuromuscular disorder with low LES tone and poor peristalsis → food stasis and esophageal dilation.

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22
Q

Achalasia types and treatment?

A

Type I: Minimal pressure
Type II: Pan-esophageal pressure (best prognosis)
Type III: Spasms (worst)
Treatments: Botox, pneumatic dilation, Heller myotomy, POEM.

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23
Q

What is Zenker’s diverticulum and its anesthesia implication?

A

Pharyngoesophageal pouch → bad breath, food retention → aspiration risk, requires RSI.

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24
Q

Hiatal hernia often coexists with what condition?

A

GERD.

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25
What kind of esophageal cancer is associated with Barrett’s and GERD?
Adenocarcinoma.
26
Key concern post-esophagectomy?
Aspiration risk for life due to altered anatomy and motility.
27
What is GERD?
Incompetence of the gastroesophageal junction → gastric contents reflux into the esophagus.
28
Symptoms of GERD?
Heartburn, regurgitation, dysphagia, nausea, 'lump in throat'.
29
What reflux substances are harmful in GERD?
HCl, pepsin, bile, pancreatic enzymes.
30
What are the 3 mechanisms of GE junction incompetence?
Transient LES relaxation, LES hypotension, Autonomic dysfunction.
31
Medical treatment for GERD?
Antacids, H2 blockers, PPIs.
32
Surgical options for GERD?
Nissen fundoplication, Toupet, LINX procedure.
33
Pre-op GERD management includes which meds?
H2 blockers (e.g. ranitidine), PPIs (night before & morning of), Sodium citrate (nonparticulate antacid), Metoclopramide (especially for diabetics, obese, pregnant).
34
When is RSI indicated?
GERD, gastroparesis, hiatal hernia, full stomach, DM, pregnancy, morbid obesity, emergency surgery.
35
What does the stomach do?
Stores, mixes, digests food into chyme, and regulates emptying into the duodenum.
36
What nerves regulate stomach motility?
PNS (vagus): Increases contractions, SNS (splanchnic): Inhibits contractions.
37
Which hormones regulate stomach motility?
Gastrin, motilin: Stimulate contractions, Gastric inhibitory peptide (GIP): Inhibits contractions.
38
What is the most common cause of upper GI bleeding?
Peptic ulcer disease (PUD).
39
What bacteria is associated with PUD?
Helicobacter pylori.
40
Symptoms of PUD?
Burning epigastric pain, worse with fasting, better with meals.
41
Treatment of PUD caused by H. pylori?
Triple therapy: 2 antibiotics + PPI for 14 days.
42
What is Zollinger-Ellison Syndrome?
Gastrin-secreting tumor → excess gastric acid → ulcers, diarrhea, and esophagitis.
43
Key pre-op consideration in Zollinger-Ellison?
Correct electrolytes, raise gastric pH, RSI due to high gastric volume.
44
What is gastric outlet obstruction and its symptoms?
Obstruction at the pyloric channel → vomiting, dehydration, metabolic alkalosis.
45
What is the main function of the small intestine?
Absorption of nutrients by mixing and exposing contents to the mucosa.
46
What movement helps the small intestine absorb nutrients?
Segmentation — contractions isolate a portion for prolonged contact with the mucosa.
47
What controls segmentation in the small intestine?
Mainly the enteric nervous system, modulated by extrinsic ANS.
48
Reversible causes of small bowel dysmotility?
Obstruction (hernias, adhesions, malignancy), ileus, electrolyte imbalance, bacterial overgrowth, critical illness.
49
Nonreversible causes of small bowel dysmotility?
Structural: scleroderma, IBD Neuropathic: pseudo-obstruction from nervous system dysfunction.
50
What are the main functions of the large intestine?
Reservoir for waste, water/electrolyte reabsorption, mass movement via giant migrating complexes.
51
When do giant migrating complexes occur?
6–10 times daily in healthy individuals.
52
Common symptoms of colonic dysmotility?
Cramping and altered bowel habits.
53
What happens to motility in IBD?
Normal contractions are suppressed by inflammation, but migrating complexes persist, worsening mucosal damage.
54
What are the two main types of IBD?
Ulcerative colitis and Crohn’s disease.
55
What part of the bowel does ulcerative colitis affect?
Colon only (mucosal layer).
56
Symptoms and labs in ulcerative colitis?
Diarrhea, bleeding, cramping, weight loss; ↑ESR, ↑PLT, ↓H&H, ↓albumin.
57
Complications of UC requiring surgery?
Hemorrhage (>6 units), toxic megacolon, colon perforation (15% mortality).
58
Where is Crohn’s disease most often located?
Terminal ileum (ileocolitis).
59
Key features of Crohn’s?
RLQ pain, diarrhea, weight loss, strictures, malabsorption.
60
What is “short bowel syndrome”?
Occurs if >2/3 of the small intestine is resected → requires TPN.
61
Medical treatments for IBD?
5-ASA Glucocorticoids for flares Abx (Rifaximin, Flagyl, Cipro) Immunosuppressants (purine analogues).
62
Where do most carcinoid tumors originate?
GI tract (95%).
63
What substances are secreted by carcinoid tumors?
Serotonin, gastrin, somatostatin, insulin, glucagon, motilin, tachykinins.
64
What is carcinoid syndrome?
Occurs when secretions reach systemic circulation → flushing, diarrhea, bronchospasm, HTN/HoTN.
65
What heart valve is most affected in carcinoid syndrome?
Right-sided valves (endocardial fibrosis).
66
Diagnosis and treatment of carcinoid syndrome?
Dx: Urinary/plasma serotonin, CT/MRI Tx: Somatostatin analogues (e.g. Octreotide), avoid triggers, serotonin antagonists.
67
What pre-op medication is used in carcinoid tumors?
Octreotide — to blunt hemodynamic effects from hormone release during surgery.
68
What are the most common causes of acute pancreatitis?
Gallstones and alcohol use (60–80% of cases).
69
How is autodigestion normally prevented in the pancreas?
Enzymes stored in inactive form, protease inhibitors, low intra-pancreatic calcium.
70
Symptoms of acute pancreatitis?
Epigastric pain radiating to back, N/V, distention, ileus, fever, HoTN.
71
Diagnostic labs and imaging for pancreatitis?
Elevated amylase and lipase; CT/MRI or endoscopic ultrasound (EUS).
72
Complications of severe pancreatitis?
Shock, ARDS, renal failure, necrosis/abscess.
73
Treatment for pancreatitis?
IVF, NPO, enteral feeds preferred over TPN, pain control with opioids.
74
Most common type of GI bleed?
Upper GI bleeding.
75
How much blood loss causes hypotension and tachycardia?
>25% blood volume.
76
What does melena indicate?
Bleeding above the cecum (upper GI).
77
Upper GI bleed: first diagnostic/therapeutic step?
EGD (endoscopy).
78
When is balloon tamponade used?
Last resort for uncontrolled variceal bleeding.
79
Common causes of lower GI bleeding?
Diverticulosis, tumors, colitis — especially in elderly.
80
What is an ileus?
Functional colonic obstruction due to loss of peristalsis without mechanical blockage.
81
Common causes of ileus?
Electrolyte abnormalities, narcotics, immobility, anticholinergics, SNS overactivity.
82
How is ileus treated?
Hydration, electrolyte correction, mobilization, NG tube, enemas, neostigmine (80–90% effective).
83
What is required during neostigmine treatment?
Cardiac monitoring due to bradycardia risk.
84
How does anxiety affect GI motility pre-op?
SNS activation → decreased motility.
85
How do volatile anesthetics affect the GI tract?
Depress electrical, contractile, and propulsive activity.
86
What is the order of GI recovery post-op?
Small intestine → stomach (~24h) → colon (~30–40h).
87
Why avoid nitrous oxide in abdominal surgery?
It expands bowel gas → increases distention.
88
Do neuromuscular blockers affect GI motility?
No — they only affect skeletal muscle, not smooth muscle.
89
How does neostigmine affect GI motility?
Increases peristalsis via cholinergic stimulation.
90
How do opioids affect the GI tract?
↓ motility, delayed gastric emptying, constipation via mu-receptor activation in enteric plexuses.

Health Assessment Exam 4 (10 decks)

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