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NA 1 > A for GI procedures > Flashcards

A for GI procedures Flashcards

1
Q

esophageal disease: symptoms

A

dysphagia
heartburn
regurgitation
pain odynophagia
globulus sensation

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2
Q

dysphagia

A
  • difficulty swallowing
  • “food stuck in chest or throat”
  • classified based on anatomical origin
  • clinical hx guides care
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3
Q

oropharyngeal

A
  • head and neck surgery
  • neurologic conditions (stroke & Parkinson’s)
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4
Q

clinical hx guides care for esophageal disease: dysphagia

A
  • better or worse with solids or liquids
  • episodic or constant
  • progressive
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5
Q

esophageal

A

mechanical
dysmotility

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6
Q

dysphagia with solid food =

A

structural/mechanical

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7
Q

dysphagia with solid and liquids

A

motility

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8
Q

mechanical disorders

A
  • benign strictures: abnormal narrowing of the esophageal lumen
  • peptic stricture
  • anastomotic stricture
  • eosinophilic esophagitis
  • post-operative fundoplication
  • radiation-induced stricture
  • esophageal ring or web
  • Schatzi ring
  • Post-endoscopic mucosal resection
    extrinsic compression from vascular structures
  • extrinsic compression from benign lymph nodes or enlarged left atrium
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9
Q

motility disorders

A
  • GERD
  • achalasia: primary is a disease of unknown etiology in which there is a loss of normal peristalsis in the distal esophagus and a failure of LES relaxation with swallowing
  • hypotensive peristalsis
  • hypertensive peristalsis
  • distal diffuse esophageal spasm
  • functional obstruction
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10
Q

malignant strictures**

A
  • mechanical disorder
  • esophageal adenocarcinoma
  • squamous cell cancer: smoke and alcohol biggest risk factors
  • extrinsic compression from malignant lymph nodes
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11
Q

esophageal motility disorders frequently present with

A

dysphagia, heartburn, or chest pain

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11
Q

the most common esophageal motility disorders are

A

achalasia, diffuse esophageal spasm, GERD

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12
Q

heart burn

A
  • burning or discomfort behind the sternum, possibly radiating to the neck
  • the relationship between heartburn and GERD → treatment for heartburn is the treatment for GERD
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13
Q

regurgitation

A

effortless return of gastric contents into the pharynx without nausea or retching

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14
Q

pain

A
  • “chest pain” - cardiac vs esophageal etiology difficult to diagnose
  • description of heartburn plus chest pain may be a result of GERD
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15
Q

odynophagia

A

pain with swallowing

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16
Q

globulus sensation

A

the feeling of “a lump in the throat”

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17
Q

achalasia

A
  • rare esophageal disorder
  • neuromuscular disorder - degeneration of ganglion cells in the myenteric plexus in the esophageal wall.
  • esophageal outflow obstruction from inadequate LES relaxation and dilated hypomotile esophagus - impaired ability of the esophagus to push food into the stomach (peristalsis) and LES to relax
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18
Q

achalasia: Symptoms

A

dysphagia (solids & liquids), regurgitation, heartburn, chest pain, long term risk of esophageal cancer

pulmonary aspiration common (pneumonia)

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19
Q

achalasia: diagnosis

A

esophagram (barium xray); EGD excludes other stuctural issues

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20
Q

achalasia: treatment

A

palliative - relieves obstruction by LES but cannot treat peristaltic deficiency of esophagus

meds: nitrates and CCB (relax LES)
- endoscopic botox injection, pneumatic dilation with EGD (most effective nonsurgical treatment), lap heller myotomy (best surgical treatment) oral endoscopic myotomy (endoscopic dividing of circular muscles of LES)

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21
Q

distal esophageal spasm (DES)/ diffuse esophageal spasm

A
  • associated with ANS dysfunction - premature and rapid propagated contraction in the distal esophagus; premature and rapid contractions are associated with esophageal bolus retention
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22
Q

distal esophageal spasm (DES)/ diffuse esophageal spasm: differential diagnosis

A

GERD, stricture, HH, functional dysphagia, opioid-induced hypomotility

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22
Q

distal esophageal spasm (DES)/ diffuse esophageal spasm: clinical manifestations

A

dysphagia and/or chest pain

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23
Q

distal esophageal spasm (DES)/ diffuse esophageal spasm: DX

A

rule out esophageal disorders (EGD with biopsy); if negative high-resolution esophageal manometry to evaluate for an esophageal motility disorder

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24
Q

distal esophageal spasm (DES)/ diffuse esophageal spasm: managment

A

relieve symptoms - primary PPI, and/or peppermint oil; secondary antispasmodic agent (hyoscyamine, dicyclomine), short-acting nitrate, phosphodiesterase enzyme inhibitor, CCB, low-dose TCA, botox injection or endoscopy/surgical myotomy

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25
Q

for patients using PDIE type 5 drugs, the reduction in SVR may result and lead to

A

hypotension, angina, and headaches, especially when taken in combination with other vasodilating medications - be aware!!

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26
Q

avoid other __ __, alpha adrenergic antagonists, during periopertaive period d/t risk of dangerously __ __

A

nitrate vasodilators; low BP

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27
Q

esophageal diverticula

A

outpouchings of the wall of the esophagus

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28
Q

esophageal diverticula: most common locations

A
  • Zenker diverticulum: pharyngoesophageal ** most common!!
  • midesophageal
  • epiphrenic (supradiaphragmatic diverticulum)
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29
Q

what does this mean??

A

ASPIRATION AND AIRWAY

  • regurgitation of food increases the risk of aspiration during anesthesia
  • cricoid pressure controversial - if the sac right behind CC may push contents into the pharynx
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29
Q

zenkers diverticulum: clinical manifestations

A
  • small or midsize Zenker are usually asymptomatic
  • large ZD are often aligned with the axis of the pharynx such that food is preferentially diverted into the diverticulum
  • when the pharyngeal sac becomes large enough to retain contents such as mucus, pills, sputum, and food, the patient may complain of halitosis, gurgling in the throat, appearance of a mass in the neck, or regurgitation of food into the mouth
  • marked weight loss and malnourishment can occur in patients with longstanding ZD
  • rarely the ZD may become so large that its retained contents may push anteriorly and completely obstruct the esophagus
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30
Q

zenkers diverticulum appears in a natural zone of weakness in the posterior hypopharyngeal wall..

A

sac-like outpouching of the mucosa and submucosa through Killian’s triangle, an area of muscle weakness between the transverse fibers of the cricopharyngeus muscle and the oblique fibers of the lower inferior constrictor (thyropharyngeus) muscle

causes significant bad breath from retention of food particles consumed up to several days previously

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31
Q

esophageal diverticula: DX

A

barium swallow evaulation

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32
Q

esophageal diverticula: differential diagnosis

A

other causes of progressive dysphagia (peptic stricture and esophageal carcinoma)

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33
Q

esophageal diverticula: management

A

surgical open or transoral approach (rigid endoscope or a flexible endoscope

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34
Q

esophageal diverticula: anesthetic implicaitons

A
  • GA is induced in the head-up position without cricoid pressure
  • empty ouch prior to anesthetic - patient applies external pressure
  • NO OGT!! perforative diverticulum
  • care with TEE
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35
Q

Hitatal hernia

A
  • herniation of part of the stomach into the thoracic cavity through the esophageal hiatus into the diaphragm
  • divided into sliding and paraesophageal
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36
Q

sliding hernia

A
  • type 1
  • GE junction and fundus of stomach slide upward; asymptomatic (no reflux); 30% of patients undergoing GI radiograph have a hernia (up to 90% with GERD)
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37
Q

paraesophageal

A

GE junction in normal place; pouch of stomach herniated next to junction

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38
Q

hiatal hernia: clincial manifestations

A
  • type 1: sliding hiatal hernias are often asymptomatic or associated with symptoms of GERD the most common which are heart burn, regurgitation, and dysphagia
  • patients with type II, III, IV hernias can be asymptomatic or have only vague, intermittent symptoms → epigastric or substernal pain, postprandial fullness, nausea, and retching
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39
Q

hiatal hernia: complications

A

volvulus (surgical emergency), bleeding, dyspnea

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40
Q

most common type of hernia

A

sliding

41
Q

hiatal hernia: DX

A

suspected with symptoms or post dissection of hx surgery, diagnosed with barium swallow, upper endoscopy, manometry, or image studies

42
Q

hiatal hernia: differential diagnosis

A

etiologies of epigastric or substernal pain, dysphagia, heartburn, or regurgitation, refractory GERD (esophagitis, esophageal motility disorder, functional dyspepsia, and CAD)

43
Q

hiatal hernia: managment

A

sliding asymptomatic - meds (GERD);
asymptomatic para esophageal - controversial
symptomatic paraesopahgeal - surgical

44
Q

esophageal tumors

A

progressive dysphagia to solid food & weight loss

45
Q

esophageal tumor: esopahgectomy

A
  • curative or palliative for tumors
  • M&M high - CV, pulmonary (ALI, ARDS), anastomotic leak, dumping syndrome, esophageal stricture, RLN injury (cervical portion of procedure)
  • patients malnourished, often chemotherapy and/or radiation
  • RISK OF ASPIRATION FOR LIFE!!
  • multimodal pain management - epidural reduces the incidence of pulmonary complications and earlier return of bowel function
46
Q

GERD

A
  • the reflux that causes bothersome symptoms, mucosal injury in the esophagus or at extraesophageal sites, or a combination of both
  • natural anti-reflux mechanism in LES and GE junction located below diaphragmatic hiatus
47
Q

GERD: DX

A
  • symptoms
  • upper GI endoscopy
  • esophageal manometry - r/o motility disorder
  • ambulatory pH monitoring
  • classified as erosive or non-erosive
47
Q

LES =

A
  • high-pressure system where the esophagus meets the stomach; protects the esophagus from highly acidic stomach secretions
  • only the lower 1/8th of esophageal mucosa tolerates stomach acid from a prolonged period
  • normal LES pressure is 30 mm Hg
48
Q

GERD: clinical manifestations

A
  • heartburn (pyrosis)
  • regurgitations (primary)
  • dysphagia, chest pain, water brash/hypersalivation, Globus sensation, odynophagia, extraesophageal symptoms (chronic cough, hoarseness, wheezing) and infrequently nausea (secondary)
48
Q

GERD: complicaitons

A
  • chronic peptic esophagitis: heartburn
  • esophagitis
  • strictures
  • ulcers
  • barret metaplasia (adenocarcinoma)
  • laryngopharyngeal reflux variant of GERD
  • gastric contents into pharynx, larynx, tracheobronchial tree > chronic cough, bronchoconstriction, pharyngitis, laryngitis, bronchitis, pneumonia
49
Q

GERD: differential diagnosis

A
  • esophagitis, pill esophagitis, and eosinophilic esophagitis

dysphagia:
- esophageal rings/webs
- impaired peristalsis d/t and esophageal motility disorder, slowly progressive dysphagia for solids with episodic esophageal obstruction is suggestive of a
- stricture or esophageal cancer (slowly progressive dysphagia for solids with episodic esophageal obstruction)
- odynophagia

50
Q

GERD: treatment

A
  • lifestyle: weight loss, HOB elevated, eliminate dietary triggers
  • pharmacologic: aim to inhibit gastric secretions
    PPI
    H2 receptor antagonists
    antacid
    surgical: Nissen fundoplication procedure
51
Q

histamine 2 receptor antagonists

A
  • decrease the secretion of acid by inhibiting the histamine 2 receptor on the gastric parietal cell
  • development of tachyphylaxis within 2 to 6 weeks of initiation if H2RAs limit their use in the management of GERD
52
Q

PPIs

A
  • potent inhibitors of gastric acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium ATPase-pump
  • most effective when taken 30 to 60 mins before the first meal of the day because the amount of H-K-ATPase present in the parietal cell is greatest after a prolonged fast
  • PPIs should be used in patients who fail twice-daily H2RAs therapy and in patients with erosive esophagitis and/or frequent (2 or more episodes a week) of severe symptoms of GERD that impair quality of life
53
Q

which is faster and more efficient? PPIs or H2RAs

A

PPIs

54
Q

GERD medication managment

A
  • antacids usually contain a combination of mag trisilicate, aluminum hydroxide, or calcium carbonate
  • mag containing antacids cause diarrhea and hypermagnesium (important with renal insufficiency); some have Na (volume overload)
55
Q

large ingestion- Ca carbonate >

A

hypercalcemia, alkalosis, acute/chronic renal injury > “milk-alkali syndrome”

56
Q

aluminum retention with renal failure >

A

nephrotoxicity and anemia

57
Q

GERD: anesthesia implications

A
  • cimetidine and ranitidine decrease gastric secretion and increase pH
  • famotidine
  • PPI
  • Na citrate (oral non-particulate antacid) increases gastric pH
  • metoclopramide (gastrokinetic agent)
58
Q

RISK OF ASPIRATION: GERD

A
  • aspiration pneumonitis 0.4 mL/kg of gastric contents aspirated and the pH of gastric contents is 2.5
  • emergent surgery, full stomach, difficult airway, inadequate anesthesia, lithotomy, autonomic neuropathy, IDDM, gastroparesis, pregnancy, increased abdominal pressure, severe illness, morbid obesity, mucosal complications…. ALL VERY IMPORTANT
  • uncontrolled symptoms - RSI with OETT
59
Q

methods to decrease risk of aspiration

A
  • aspiration risk with NPO or certain medical conditions (important with GI procedures)
  • the most signif factor in determining aspiration severity is the pH of the aspiration
  • a pH less than 2.5 usually correlates with worse outcomes
  • volume is also a factor; 0.4 mL/kg of aspirate correlates with worse outcomes
60
Q

what do we want to do to decrease risk of aspiration?

A

increasing gastric emptying/prokinetics

61
Q

metoclopramide

A

is a dopamine antagonist that enhances LES tone, increases gastric emptying, and thereby decreases gastric volume > gut motility stimulator and antiemetic

62
Q

a dose on 10mg has an onset of

A

30-60 mins oral and 2 mins IV

63
Q

when is metoclopramide contraindicated?

A

in patients with Parkinson’s disease, pheochromocytoma, GI obstruction, or in patients taking meds that may interact and cause extrapyramidal side effects

64
Q

famotidine (Pepcid)

A

and H2RA decreases volume and acidity when given a few hours before surgery

65
Q

acidity of gastric contents can be __ by H2-receptor antagonsists and __, which can also decrease gastric volume

A

decreased; PPIs

66
Q

increasing pH and decreasing the volume of gastric contents

A

PPI, including omeprazole and lansoprazole, are most effective when given in two repeated doses, the night before and morning of surgery

67
Q

Sodium citrate

A
  • nonparticulate antacid that can be given orally within an hour preoperatively to increase gastric pH above 2.5
  • its effect on increasing pH is more rapid than H2-receptor antagonists and PPI, which may be more useful in an emergency case
68
Q

lower LES tone **

A

anticholinergic agents (glyco, atropine)
opioids
thiopental/benzo
propofol/dex
inhaled anesthetics
cricoid pressure
NG tube
alkalinization
protein feeding
beta agonists

68
Q

increased LES tone **

A

antiemetics
succinylcholine
NMBD
cholinergic agents
antacids

69
Q

no effect on LES tone **

A

atracurium
vecuronium
H2 antagonists
sleep

70
Q

peptic ulcer disease

A
  • a peptic ulcer is a defect in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the wall
  • peptic ulcers may present with dyspepsia (indigestion) or other gastrointestinal symptoms or may be initially asymptomatic and then present with complications such as hemorrhage or perforation
71
Q

peptic ulcer disease: clinical manifestations

A
  • asymptomatic (70%)
  • abdominal pain (upper abdominal pain/discomfort*; “epigastric”, radiation to the back) → duodenal ulcers - 2-5 hrs after a meal and at night
  • dyspepsia, bloating, abdominal fullness, nausea, GERD
72
Q

peptic ulcer disease: differential diagnosis

A
  • other causes of dyspepsia such as drugs, biliary disease, gastric malignancy, chronic pancreatitis
  • excluded by upper endoscopy
72
Q

peptic ulcer disease: imaging

A

abdominal CT- focal discontinuity of mucosal hyperenhancement and luminal outpouching; gastric wall thickening, inflammation, mucosal enhancement

73
Q

peptic ulcer disease: labs

A

anemia - with bleeding
perforation - leukocytosis

74
Q

peptic ulcer disease: DX

A
  • suspected in patients with dyspepsia, especially in the setting of NSAID use or a hx of H. pylori infection
  • suspected based on imaging
  • definitive diagnosis visualization of the ulcer on upper endoscopy
74
Q

what is often the cause of PUD? percentage of which is duodenal vs. gastric ***

A

H. pylori

the patient will often go on abx
(90% of duodenal ulcers, 75% of gastric ulcers

75
Q

PUD: complications ***

A
  • acute upper GI hemorrhage - presents with nausea, hematemesis, melena
  • gastric outlet obstruction
  • penetration and fistulization
  • perforation
76
Q

PUD: treatment ***

A
  • antacids - symptomatic relief
  • H2RA’s (famotidine/ranitidine/cimetidine (binds to CP450) - inhibit gastric acid secretion
  • PPI (omeprazole) - irreversibly inhibit H,K ATPase inhibits CP450/fastest and most potent acid inhibitor
  • prostaglandin analogs (misoprostol) - maintain mucosal integrity by enhancing bicarbonate secretion stimulating mucosal blood flow and decreasing mucosal turnover
  • cytoprotective agents (pesto) - coats ulcer
  • surgical = vagotomy > stops vagus nerve from causing acid release but results in delayed gastric emptying
77
Q

inflammatory bowel disease comprised of two major disorders

A
  • ulcerative colitis → affects the colon
  • Crohn disease → involves any compartment of GI tract mouth to perianal
78
Q

ulcerative colitis

A
  • relapsing and remitting episodes of inflammation limited to the mucosal layer of the colon > continues distribution of disease
  • generally, involves rectum > rectal bleeding
  • diarrhea
  • abd pain mild to moderate
79
Q

Crohn Disease

A
  • transmural inflammation and skips areas of involvement > inflammation leads to fibrosis and strictures with obstructive symptoms (fissures and abscesses)
  • most commonly affects the distal ileum and proximal large colon
  • diarrhea
  • moderate to severe abdominal pain, diarrhea (with or without rectal bleeding), fatigue and weight loss
80
Q

carcinoid tumors

A
  • “carcinoid” well-differentiated neuroendocrine tumors (NETs) originating from the GI tract*, lungs, kidneys, or ovaries
  • tumors composed of enterochromaffin cells (Kulchitsky cells)
  • modern > NET for tumors originating in GI tract or “neuroendocrine carcinoma”
80
Q

carcinoid syndrome

A

result of secretion of serotonin and vasoactive substances into systemic circulation in the setting of neuroendocrine tumor

primary = serotonin, histamine, kallikrein

81
Q

carcinoid syndrome: symptoms

A

chronic flushing and/or diarrhea typical manifestation of carcinoid syndorme

82
Q

carcinoid syndrome: treatment

A

medical managemnet = octeotride: long acting synthetic analogues of somatostatin

surgical = complete excision of tumor with bowel resection and lymphadenectomy

83
Q

carcinoid crisis

A
  • caution.. anesthesia may precipitate carcinoid crisis
  • manipulation, chemical stimulation or tumor necrosis may also cause a crisis
  • GOAL = prevent release of bioactive mediators by avoiding triggers
84
Q

carcinoid crisis: clinical manifestations

A
  • severe flushing (cutaneous/facial)
  • dramatic changes in BP (hypotension)
  • tachycardia
  • bronchoconstriction (wheezing & dyspnea)
  • mental status changes
  • diarrhea
85
Q

carcinoid crisis: anesthetic implications

A
  • may occur at induction or at any time in the perioperative period
  • pretreat with octreotide or lanreotide and continue through the perioperative period (CRISIS = 150-200 mcg 4-6 hrs 24-48 hrs before and through surgery
  • invasive monitoring (arterial line)
  • optimize fluid and electrolytes
  • block H1, H2 and serotonin receptors
  • provide anxiolysis
  • avoid histamine-releasing agents and succinylcholine
  • avoid sympathomimetics
  • treat hypotension and alpha-agonist (phenylephrine) or vasopressin
  • maintain normothermia
  • monitor plasma glucose
86
Q

carcinoid crisis: drugs

A
  • avoid drugs that release histamine (morphine, meperidine, codeine, atracurium, vanco, hyperosmotic agents)
  • AVOID SUCC > An increase in intraabdominal pressure and fasciculations may trigger mediator release
  • propofol has a profound effect suppressing the
    sympathetic response to intubation
  • avoid sympathomimetics > ketamine
87
Q

carcinoid crisis: A

A

balanced technique with GA OEYY, PPV, inhalation agent, NDMR (roc or vec), opioid (fentanyl), N2O safely

88
Q

preoperative anesthetic considerations with carcinoid tumor:

A
  • benzo to reduce anxiety
  • antihistamine to reduce histamine rleease
  • octreotide for symptomatic relief and prevention of perioperative hypotension
  • optimize fluid and electrolytes
  • placement of invasive lines prior to induction (arterial line and or pulmonary artery catheter with coexisting cardiac dysfunction)
89
Q

acute pancreatitis

A
  • inappropriate activation of trypsin leads to activation of protease-activated receptor-2 (PAR2) and activation of other pancreatic enzymes
  • it results in out-of-proportion inflammation of the pancreas leading to a systemic inflammatory response syndrome (SIRS) - like response
90
Q

acute pancreatitis: symptoms

A
  • abd pain typically radiating to the back
  • nausea, vomiting
  • abd distention
  • jaundice
  • fever
  • tachycardia
  • hypotension
  • cullen’s sign (hemorrhagic discoloration of the umbilicus)
  • grey- turner’s sign (hemorrhagic discoloration of the flanks)
91
Q

acute pancreatitis: causes

A
  • gallstones (triggered by obstruction of the duct)
  • trauma (postop, post-ERCP)
  • abd medications ( steroids, NSAIDs, diuretics)
  • autoimmune
  • infection
  • metabolic (hypercalcemia, hypothermia)
  • hypertriglyceridemia
  • pancreatic tumors
92
Q

acute pancreatitis: lab values

A
  • CRP will be high (> 150 in first 72 hrs indicates severe/necrosis)
  • amylase - high
  • lipase - high (> 3 x normal)
93
Q

chronic pancreatitis: most common etiology

A

diagnostic triad: steatorrhea, pancreatic calcification, DM

94
Q

acute pancreatitis: complications

A

shock
hypoxemia/ARDS (20%)
renal failure (25%)
DIC
infection of necrotic pancreatic material (50% material)
vomiting > hyperchloremic alkalosis

95
Q

acute pancreatitis: treatment

A
  • aggressive fluids (immediate) > fluid loss into the peritoneum causes hemoconcentration and hypovolemia
  • electrolyte resuscitation (immediate)

oral fluids?
TPN?
intubation for ARDS

96
Q

chronic pancreatitis

A
  • permanent and irreversible damage to the pancreas with inflammation, fibrosis, and destruction of exocrine and endocrine cells

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