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Boards: GI > GI Dysmotility in CC. Whitehead. 2016. JVECC > Flashcards

GI Dysmotility in CC. Whitehead. 2016. JVECC Flashcards

1
Q

What are established risk factors for GIDM in critically ill people:

A
  • mechanical ventilation
  • sepsis, shock, trauma, systemic inflammatory response syndrome [SIRS], and multiple organ failure
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2
Q

Name substances that excite the motor neurons in the GI wall:

A
  • acetylcholine (Ach),
  • tachykinins (particularly substance P and neurokinin A)
  • serotonin (5-hydroxytryptamine [5-HT])
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3
Q

Name substances that inhibit the motor neurons in the GI wall:

A
  • vasoactive intestinal peptide (VIP),
  • somatostatin
  • nitric oxide (NO)
  • gamma-amino butyric acid (GABA)
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4
Q

What is the primary neurotransmitter of the GI tract promoting GI motility and what nerves supply it?

A
  • Acetylcholine (Ach)
  • Parasympathetic innervation mainly via the vagus and pelvic nerves + other preganglionic parasympathetic fibers (including ENS)
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5
Q

What is the primary neurotransmitter of the GI tract inhibiting GI motility and where does it work?

A
  • Norepinephrine
  • acts indirectly on neurons of the enteric system (ENS) and directly on muscles and glands
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6
Q

Explain the interdigestive motility complex. What is its function, how is it generated and regulated?

A
  • Alternate form of motility clearing indigestible materials (“housekeeping” function)
  • Involves the migrating motor complex (MMC) in dogs: pyloric relaxation, strong antral wave of peristalsis, moves indigestible material into the duodenum
  • MMCs are regulated by the enteric nervous system (ENS) and modulated directly by regulatory peptides including somatostatin, motilin, and pancreatic polypeptide.
  • MMCs occur at a rate of 15 to 20 per minute
  • Ingestion of a meal will interrupt the interdigestive motility and digestive motility pattern starts
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7
Q

What is the difference between canine and feline interdigestive motility?

A
  • Interdigestive motility in dogs involves the migrating motor complex (MMC) and giant migrating complexes in cats
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8
Q

How do the muscle fibers differ between the feline and canine esophagus?

A
  • Canine esophagus is entirely made of striated muscle fibers
  • Feline esophagus has a distal portion of smooth muscle fibers
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9
Q

How are the different muscle fibers regulated?

A
  • Striated muscles of the esophagus are regulated through the vagus nerve
  • Smooth muscle fibers are innervated through the ENS, and indirectly through the autonomic nervous system
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10
Q

What substances have been shown to affect esophageal motility?

A
  • NO
  • Somatostatin
  • Motilin
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11
Q

Explain adaptive and receptive relaxation of the stomach

A

Receptive relaxation

  • induced by chewing and swallowing
  • regulated through a vago-vagal reflex

Adaptive relaxation

  • relaxation of muscles when food enters the stomach
  • inhibitory vagal fibers à Ach release à activation of inhibitory enteric pathways à release of NO, VIP, ATP à muscle relaxation
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12
Q

What are the steps of gastric emptying?

A
  1. Relaxation of the fundal portion of the stomach
  2. Antral Peristalsis
  3. Opening of the pyloric diameter
  4. Relaxation of the duodenum
  5. Contraction of the duodenum
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13
Q

Describe the enterogastric reflex. What is it stimulated by?

A
  • Inhibits further gastric emptying into the duodenum when the duodenum is “full”
  • inhibits the vagal nuclei of the medulla and local reflexes while activating sympathetic fibers à cause the pyloric sphincter to tighten, delaying gastric emptying.
  • activated by a low pH, high osmolality, and the presence of high lipid content. (+ distention of the duodenum?)
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14
Q

What are the 5 main contractile patterns of the small intestines?

A
  • peristaltic waves
  • stationary segmenting contractions
  • giant contractions (aboral)
  • stationary or migrating clusters of contractions
  • MMCs
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15
Q

What is the average small intestinal transit times in dogs versus cats?

A
  • 3-5 hours in dogs
  • 2-3 hours in cats
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16
Q

What are the types of colonic contraction?

A
  • short duration phasic contractions amidst a background state of persistent colonic tone.
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17
Q

How does mechanical ventilation affect esophageal motility?

A
  • Shown to reduce the frequency, amplitude, and percentage of propulsive contractions of the esophagus
  • Gastroesophageal reflux from relaxation of the lower esophageal sphincter
  • Inhibition of esophageal motor activity from medications such as benzodiazepines, opioids, ketamine
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18
Q

The pathophysiology of delayed gastric emptying in critically ill animals and people is not fully understood. Describe the two most important theories?

A

“pump failure”

  • Primary motor dysfunction
  • Decreased antral motility and display of the fasting motility pattern during feeding.

“excessive feedback” theory

  • disproportionate activation of an inhibitory feedback pathway originating in the proximal small intestine or duodenum
  • based on the nutrient release of neuroendocrine peptides such as cholecystokinin (CCK) and 5-HT (via 5-HT3 receptors), which subsequently inhibit vagal and spinal afferent neurons and result in delayed gastric emptying
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19
Q

GI inflammation is an implicated cause for functional ileus of the small intestines. What is the presumed pathophysiology?

A
  • During GI inflammation, leukocytes (particularly neutrophils) à releasing proteolytic enzymes and cytokines à damage the muscle layer of the GI tract directly
  • inflammatory mediators à release of NO à paralysis of the muscular cells à propagation of intestinal dilation.
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20
Q

Explain how migrating motor complex disturbances may lead to bacterial overgrowth and translocation

A
  • people: increase in quiescent period (phase I), decrease in intermittent contractions (phase II), increase in high amplitude regular contractions (phase III) but these are retrograde
  • reduce expelling of the luminal contents, including bacteria and food particles, into the colon
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21
Q

Is megacolon in cats associated with critical illness?

A

Not usually, megacolon is considered an end-stage condition of a chronic disease process rather than an acute critical illness

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22
Q

What is Ogilvie’s syndrome?

A
  • affiliated with an autonomic imbalance, an impaired pelvic parasympathetic innervation, and a predominance of inhibitory sympathetic tone.
  • acute colonic pseudo-obstruction
  • has been associated with gut ischemia, systemic or local inflammation, and sepsis.
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23
Q

What conditions have been shown to secondarily cause GIDM?

A
  • Acute stress (e.g., noise stress, TBI)
  • Inflammation of the viscera (e.g., pancreatitis, mesenteritis, peritonitis)
  • Electrolyte derangements (hypokalemia, hypermagnesemia, and hyper- or hypocalcemia)
  • Metabolic disturbances (e.g., acidosis, hypoadrenocorticism, hepatic encephalopathy, uremia)
  • Drugs (opioids, dopamine, alpha-2-adrenergic agonist)
  • diabetic gastro-neuropathy
  • splanchnic hypoperfusion
  • hypoxemia
  • obesity
  • SIRS or sepsis
  • Neoplasia
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24
Q

How do opioids lead to GIDM?

A
  • have been shown to inhibit GI transit by reducing Ach release and altering neuronal excitability (Ach main neurotransmitter for GI motility!)
  • may also increase smooth muscle activity → BUT inhibit coordinated propulsive peristalsis à disordered nonpropulsive contractile activity
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25
Q

Explain the pathophysiology of GIDM in diabetes mellitus.

A

may include diabetes-associated neuropathy, hypoglycemic and hyperglycemic effects on GI motor function, and insulin’s effect on GI motility

  • autonomic neuropathies and vagal nerve dysfunction
  • Hyperglycemia has been shown to reduce gastric antral contractions, suppress interdigestive phase III activity, and impair gall bladder emptying
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26
Q

Name 3 mediators shown to cause GIDM in patients with MODS and sepsis

A
  1. Tumor necrosis factor
  2. VIP (vasoactive intestinal peptide)
  3. NO
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27
Q

What are proposed reasons for post-surgical GIDM

A
  • mechanical manipulation of the bowel
  • inflammation → GI inflammation may affect increased sympathetic efferent activity via the splanchnic nerves, resulting in an overall shift toward decreased gut motility in postoperative ileus
  • pain
  • hormonal factors (eg, substance P, VIP, NO)
  • concurrent medications (especially opioid medications)
  • electrolyte disturbances.
28
Q

List consequences associated with GIDM

A
  • gastroesophageal reflux
  • esophagitis
  • aspiration
  • bacterial overgrowth
  • bloating or distension of the GI tract leading to increased IAP
  • fluid sequestration and hypovolemia
  • delay of nutritional delivery
29
Q

List clinical signs associated with GI dysmotility

A
  • anorexia
  • abdominal pain
  • abdominal distension
  • nausea, vomiting
  • increased volume of gastric residual volumes (GRVs)
30
Q

Explain the self-exacerbating cycle of GI dysmotility and hypovolemia

A
  • GI dysmotility > gastrointestinal distention > rise in intraabdominal pressure > compromises intestinal perfusion and microcirculation > fluid sequestration into the intestinal wall and lumen > hypovolemia and further microcirculatory impairment > more dysmotility
  • Dysmotility > unabsorbed nutrients in the intestinal lumen > osmotic diarrhea > further fluid loss > …
  • > hypovolemia and further microcirculatory impairment
  • Inflammation of the intestines > fluid loss into the lumen
31
Q

List the limitations of radiography to assess for GIDM

A
  • inability to identify subtle motility disorders
  • administering food with barium or barium to anorectic patients
  • risk of aspiration of food and barium
32
Q

List the limitations of ultrasonography to assess for GIDM

A
  • inherent subjectivity
  • no published/established reference ranges for normal motility on ultrasonography
33
Q

Discuss how well Gastric residual volume measurements can be used to guide treatment strategies of patients with GIDM

A
  • one study on dogs found no direct association between GRV, the occurrence of vomiting or regurgitation, or incidences of aspiration
  • Therefore, the use of GRV to guide treatment strategies should be approached with caution until additional studies have been conducted.
34
Q

Lists specialized tests that may be utilized to assess GI motility

A
  • Radioscintigraphy
  • C-breath test (C-acetate validated in dogs)
  • Lactulose breath test
  • Manometry
  • Tracer studies
  • MRI
35
Q

List the mainstay of treatment for GIDM

A
  • Identify and treat the predisposing illness
  • Early nutritional intervention
  • Judicious fluid therapy
  • Early ambulation
  • Correction of metabolic derangements
  • Maintenance of normothermia
  • Multimodal pain management
  • Pharmacologic intervention
36
Q

What are the proposed mechanisms supporting early enteral feeding in critically ill patients?

A
  • improving blood flow to the gut
  • protecting the GI mucosa
  • reducing the risk of translocation of intestinal bacteria
  • stimulating motility
  • promoting secretion of various gut hormones and growth factors
37
Q
A
38
Q

In a study of critically ill and mechanically ventilated patients, how was early enteral nutrition associated with survival?

A
  • EN within 48 hours was associated with a 20% decrease in mortality in ICU patients and 25% for hospital mortality
39
Q

What are the detrimental effects of fluid therapy on GI integrity?

A
  • Rat studies showed that GI edema induced by fluid therapy led to increased transit time, increased intestinal permeability to macromolecules, and decreased tissue resistance
40
Q

What is the proposed cellular mechanism of gut edema leading to GIDM?

A

Incompletely understood

nuclear factor kappa B >

  • trigger a gene regulation program leading to decreased myosin light-chain phosphorylation and > decreased intestinal contractile activity

increased expression of inducible NO synthase and subsequent NO production

  • upregulates smooth muscle cyclic guanosine monophosphate (cGMP) > impeding myosin light chain phosphorylation and actin/myosin cross-linking > deterring smooth muscle contractility
41
Q

what is the evidence supporting early ambulation to reduce ileus in veterinary patients?

A
  • There are no veterinary studies supporting early ambulation postoperatively to prevent or treat ileus
  • Human studies have not found a difference in occurrence of ileus, but early ambulation is still recommended, more so due to shown decrease of risk for postoperative respiratory and thrombotic complications
42
Q

What is the difference between morphine and fentanyl on their effect on GI motility?

A
  • Morphine requires much lower concentrations to cause GI ileus whereas fentanyl requires similar concentrations for analgesic effects and ileus
43
Q

Study results on the effect of vasopressin on GI motility are conflicting. What are the proposed mechanisms?

A
  • motility modulating effects could have resulted from vasopressin-mediated stimulation of sodium chloride and water absorption, as well as inhibition of chloride secretion
  • may act as a neuromodulator of enteric cholinergic neurons inducing excitatory effects on the contractility via V1a receptors.
44
Q

By what mechanism do both metoclopramide and domperidone increase GI motility. Explain this mechanism and its pathways. Discuss the efficacy of this pathway for prokinetic effects.

A
  • Dopaminergic receptor (D2) antagonism (both)
  • D2 receptors of the post-ganglionic cholinergic neurons in the myenteric plexus (s. picture)
  • When activated > these cholinergic neurons will reduce Ach release > decreased peristalsis
  • When deactivated (D2 antagonisms) > increased release of Ach à increased peristalsis
  • Controversial whether dopaminergic effects contribute to GI contractility
45
Q

Besides dopaminergic antagonism, what pathway contributes to domperidone’s prokinetic effect. Compared to dopaminergic antagonism, how effective is this pathway.

A
  • Alpha2 and beta2 adrenergic antagonism (domperidone)
  • Decreased sympathetic tone will lead to increase in Ach
  • Alpha2 and beta2 agonism directly inhibits GI motility > decrease inhibition à increased motility
  • Prokinetic effects likely owing more to adrenergic antagonism than dopaminergic antagonism
46
Q

How well is domperidone established as a prokinetic agent?

A
  • Effect on motility controversial
  • Shown to actually dyscoordinate motility
  • Does not work on LES, will not help with gastroesophageal reflux
  • No documented small intestinal effects on transit
47
Q

Besides prokinetic effects, what does domperidone work well for? How does it compare to metoclopramide?

A
  • Antiemetic effect
  • Works better than metoclopramide for antiemetic effects (12-25 times stronger)
48
Q

Explain how the pathway of serotonin-receptor agonists increase GI motility

A
  • Mainly implicated in increasing GI motility: 5HT-4 (secreted by GI mucosa)
  • 5HT-4 receptor agonists will increase its presynaptic activity > stimulates Ach release from postganglionic cholinergic neurons > smooth-muscle contraction
  • 5HT-1 and -3 receptors also implicated in having effects on GI motility
49
Q

What are the common veterinary serotonin-receptor agonists used to increase GI motility?

A
  • Metoclopramide
  • Cisapride
50
Q

What serotonin receptors are commonly targeted to decrease vomiting and nausea. Is this via antagonism or agonism and what common veterinary medications have this effect?

A
  • 5HT-1 and -3 receptor antagonism reduces nausea and vomiting
  • Ondansetron, Dolasetron, Erythromycin, Cisapride, Metoclopramide
51
Q

List the locations of the GI tract where Cisapride has shown to increase motility

A
  • Esophagus in animals with smooth muscles in the esophagus (cats, not dogs)
  • Gastroesophageal sphincter pressure
  • Stomach
  • Antropyloroduodenal coordination
  • Jejunum
  • Colon
52
Q

What complications of Cisapride lead to its withdrawal from the human market, and have been shown in induced canine models, but not small animal veterinary patients?

A
  • QT interval prolongation and slowing of cardiac repolarization via a blockade of the rapid component of the delayed rectifier potassium channel
53
Q

Through what mechanism of action does metoclopramide act as an antiemetic

A
  • Through dopaminergic and 5HT-3 receptor antagonism > prevents stimulation of the chemoreceptor trigger zone
54
Q

Through what mechanism of action does metoclopramide act an a prokinetic?

A
  • 5HT-4 receptor agonism > increased presynaptic activity > stimulates Ach release from postganglionic cholinergic neurons > smooth-muscle contraction
  • Dopaminergic receptor antagonism > unclear whether this works, likely more reliant on 5HT-4 pathway
55
Q

List the locations of the GI tract where Metoclopramide has shown to increase motility. Where does metoclopramide not work?

A
  • Lower esophagus (cats, not dogs)
  • Stomach (gastric emptying)
  • Antropyloroduodenal coordination
  • Not documented to work in the distal small intestines or colon
56
Q

What are the main side effects of metoclopramide and how are they treated?

A
  • “Extrapyramidal signs” > motor restlessness, involuntary muscle spasms, inappropriate aggression
  • Treat symptomatically with antihistamines, benzodiazepines, beta-adrenergic antagonists, dopamine agonists
57
Q

What are the main veterinary drugs used for their motilin receptor agonism?

A
  • Erythromycin and Azithromycin
58
Q

Explain how motilin stimulates GI motility

A
  • Motilin is a peptide synthesized by endocrine cells of small intestinal mucosa
  • Motilin receptors are located on cholinergic nerves, and they have been isolated from the smooth muscle of the GI tract
  • Regulates interdigestive MMCs > phase III
59
Q

Through which receptors does erythromycin act to increase GI motility in dogs versus cats?

A
  • In both animals erythromycin mimics the effects of motilin on the upper GI tract and increases motility
  • In dogs this happens indirectly through 5HT-3 cholinergic pathways
  • In cats this happens directly through stimulation of motilin smooth muscle receptors
60
Q

List the locations of the GI tract where erythromycin has shown to increase motility.

A

Upper GI tract

  • Esophagus (cats)
  • Stomach
  • Small intestines
61
Q

Explain whether you can use Erythromycin in the same animal for both its antimicrobial and prokinetic effects.

A
  • Cannot be used for both effects in the same animal:
  • Prokinetic effects are achieved at lower dosages, which are microbially ineffective
  • Larger, antimicrobial dosages have shown to cause retrograde peristalsis
62
Q

What are the side effects of erythromycin? Are these more commonly seen when used as a prokinetic or as an antimicrobial?

A
  • Q-T prolongation, nausea, inappetence > at higher dosages (antimicrobial)
  • Low dose (prokinetic) well tolerated
63
Q

How are histamine receptors supposedly involved in GI motility? What is the current therapeutic target?

A
  • Histamine 1 receptor activation causes contraction by increasing Ca-availability
  • Histamine 2 receptor antagonism inhibits acetylcholine esterase > more Ach available > enhances and prolongs effects of Ach on smooth muscle contractions > increased motility
  • Drugs used include ranitidine and nazitidine
64
Q

What locations of the GI tract have ranitidine and nazitidine shown to work?

A
  • Stomach
  • Ileus
  • Colon
65
Q

Explain potential strategies to reduce the effects of opioids on GI motility. Why is this commonly not achievable/feasible?

A
  • Mu-antagonists, e.g., naloxone, alvimopan
  • Oral naloxone has only limited bioavailability
  • Alvimopan à antagonize the inhibitor effects of opioids on gut motility but do not cross the blood-brain barrier and therefore do not antagonize the analgesic effects
  • BUT very expensive! (1000 $ per treatment)

Boards: GI (2 decks)

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