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Boards: GI > GI Physiology > Flashcards

GI Physiology Flashcards

1
Q

Monogastric Species

A

Dogs, Cats, Pigs (spiral colon)

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2
Q

Ingesta Travel through Ruminants

A

large rumen on L side –> reticulum –> omasum –> abomasum (functional stomach)

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3
Q

Rumen Function

A

Motility controlled by medullary gastric center in brain

Ruminations 1-3/min

Depression, pain, fear, pyrexia, endotoxemia, hypocalcemia, rumen tympany – reduction in motility

Rumen pH changes DT saliva, plasma, rumen

Salivary glands
* Parasympathetic: serous volumes from parotid
* Sympathetic: mucous

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4
Q

Gas Production in Sheep

A

5L/hr

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5
Q

Gas Production in Cattle

A

30L/hr

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6
Q

UES

A

cricopharyngeal, pharyngeal constrictor m
 Supplied by vagus N
 Normally closed to avoid entrainment of air

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7
Q

LES

A

not anatomically defined structure, functionally defined
 increased intraluminal pressure 15-25mmHg
 Numerous NTs, hormones involved in control

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8
Q

Esophageal M composition - dogs

A

striated m

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9
Q

Esophageal M composition - other species

A

Horse, cow, pig, primates: prox 2/3 striated, distal 1/3 SmM

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10
Q

Camelids

A

3 compartments = C1 (glandular), C2, C3 (true stomach)

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11
Q

Structure of GIT

A

o Mucosa
o Submucosa
o Muscularis muscle – inner circular layer, outer longitudinal layer
o Serosa – thin membrane, secretory cells – produce/secrete serous fluid

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12
Q

Enteric NS

A
  1. Extrinsic components
  2. Intrinsic = myenteric, submucosal plexuses (SMP)
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13
Q

Myenteric Plexus

A

btw circular, longitudinal m layers – controls intestinal motility

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14
Q

Submucosal Plexus

A

btw submucosa, inner circular m layers – coordinates motion of luminal epithelium

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15
Q

SMP Preganglionic Neurons and Fibers

A

Preganglionic PSNS neurons: long fibers that synapse with ganglia of myenteric or SMP neurons within GIT

Preganglionic SMP fibers synapse with ganglia just outside GIT
 NT: release ACh

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16
Q

SMP Postganglionic Neurons, Fibers

A

o Postganglionic SMP neurons travel into GIT, synapse with intrinsic plexuses, directly onto R in intestine
 Utilize ACh, substance P, vasoactive intestinal peptide, neuropeptide Y, gastrin-releasing peptide
 NT: release NE

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17
Q

Extrinsic ENS

A

PSHS innervation to upper, lower GIT via Vagus (upper), pelvic (lower) N; SNS via SC segments T1-L3

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18
Q

Swallowing Reflex

A

Swallowing center in medulla, pons – phases mediated by vagus N
 Oral, pharyngeal, esophageal phases

Pharyngeal innervation: recurrent and laryngeal N (cricopharyngeal m), pharyngeal branch of vagus N/glossopharyngeal m (mucosa)

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19
Q

Two Patterns of Muscular Activity with GIT

A
  1. Migrating Motor Complexes (MMCs)
  2. Digestive pattern when food enters stomach
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20
Q

Migrating Motor Complexes

A

–Fasting conditions
–Dogs, humans
–Interstitial cells of Cajal, located within myenteric plexuses, specialized PM cells that create, maintain MMCs

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21
Q

MMC MOA

A
  • ‘Slow waves’ of depolarization, spread via gap junctions btw SmM cells over large sections of intestine
  • Remain below depolarization threshold for propulsive ctx
  • Housekeeping: move residual fluid, mucus, bacteria, cellular debris aborally (away from mouth) during interdigestive period
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22
Q

Cats and MMCs

A

migrating spike complex, weaker than MMC

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23
Q

Digestive pattern when food enters stomach

A

Electrical activity increases as food enters stomach – initiation of digestive pattern

Sphincters, secretions of intestine in path of bolus relax to allow entry

Ingesta mixed, moved along GIT via circular (mixing), longitudinal (movement) muscles with feedback inhibition
* Longer, more thorough contact for digestion

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24
Q

Effect of Nervous System on GI Motility

A

o SNS: inhibitory
o PSNS: excitatory – ACh, SP = contraction, VIP/NO = relaxation

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25
Q

Changes in GIT Assoc with Pregnancy

A

Circulating progesterone
 Decreased gastric pH: affects Tmax, Cmax of PO drugs
 GI motility decreased
 LES tone decreased

Cranial displacement of stomach by gravid uterus
 Increased risk of regurgitation, aspiration

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26
Q

Effects of Ax on GIT Function

A

o Changes in saliva production
o Nausea, vomiting, regurgitation
o Ileus, constipation - tympany, POI
o GER
o Reduced secretion of digestive fluids
o Aerophagia (assoc with panting)
o Diabetic patients: gastroparesis, delayed gastric emptying secondary to autonomic neuropathy
o Stress of dz, hospitalization: predisposed to GI dysfunction, esp gastric ulceration, diarrhea

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27
Q

Most significant perianesthetic GIT complication?

A

pulmonary aspiration, esophagitis following vomiting, regurg, GER
o Aspiration = pneumonitis, pneumonia, severe hypoxemia
o Esophagitis = stricture of esophageal lumen  persistent vomiting, regurg, dysphagia, WL, debilitation

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28
Q

Which NT stimulate vomiting?

A

Serotonin (5HT, 5HT3), histamine, ACh, dopamine, neurokinin 1 (NK-1), substance P

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29
Q

Other Stimulations for vomiting

A

cerebral cortex (anxiety, anticipation), vestibular apparatus (motion sickness), local damage to/distension of GIT via release of serotonin or stimulation of vagal afferent neurons

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30
Q

CRTZ

A

Area of brainstem in area postrema

  • When stimulated, send signals to vomiting center via D2 receptors 5-HT3 receptors primarily but also ACh, Opioids, and Substance P
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31
Q

Area Postrema

A

circumventricular organ

highly vascularized structure that lacks a true BBB (but receives blood directly from systemic circulation)

sensitive to presence of some drugs and toxins in blood or products of inflammation

When stimulated, send signals to vomiting center via D2 receptors 5-HT3 receptors primarily but also ACh, Opioids, and Substance P

32
Q

Vestibular System

A

within temporal lobe

Changes in equilibrium, CN 8 afferents via H1/muscarinic AChR to vomiting center

33
Q

Cortex

A

Anticipatory/anxiety-induced vomiting originates in cerebral cortex

Also increased ICP, meningial irritation

Via GABA, H1

34
Q

Communication from GIT

A

Enterochromaffin cells in GIT release serotonin&raquo_space; Stims vagal afferents (CN 10) that terminate in CRTZ to communicate info about intestinal luminal compounds and gastric tone via serotonin 5-HT3 receptors

35
Q

Stretch, mechano R in GI

A

 Mechanoreceptors in pharynx + Tension receptors / Chemoreceptors in stomach, duodenum&raquo_space; stimulation sends signals to VC in BS
* GOAL: noxious tactile or chemical stimulation in GI mucosa results in clearance of offending stimulus

36
Q

Three Phases of Vomiting

A
  1. Projection Phase
  2. Retching Phase
  3. Ejection Phase
37
Q

Projection Phase

A
  • Nausea, reverse peristalsis of SI –> pushes proximal small bowel contents back into stomach
  • Secretion of saliva via PNS, tachycardia via SNS
38
Q

Retching Phase

A

Deep inspiration, closure of glottis to protect trachea from aspiration

Rhythmic ctx of ICM/diaphragm/abdominal M against closed glottis to mix contents of stomach, SI
o Mixing increases pH of gastric contents
o Increased intrathoracic pressure (deep inspiration) compresses esophagus, prevents orad expulsion of contents

39
Q

Ejection Phase

A
  • Continued glottic closure
  • Contraction of pylorus, relaxation of LES/esophagus
  • Sudden dramatic increase in abdominal pressure from abdominal mm contraction + decrease in thoracic pressure –> pushes gastric contents out of stomach, into esophagus
  • Soft palate occludes nasopharynx
  • Reverse peristalsis in esophagus expels contents out UES
40
Q

Fasting: Adult SA

A

:4-6hr food, unlimited water; 2-4hr in diabetics (1/2 insulin 2-4hr prior)
 High risk for regurg: consider 6-12hr fast, water withhold 6-12hr

41
Q

Fasting: Pediatric SA

A

<8wk, <2kg: no longer than 1-2hr

42
Q

Fasting: Adult Bovids

A

feed 24-48hr, water 6-12hr

43
Q

Fasting: calves, SR, camelids

A

feed 12hr, water 6-8hr; LJ = 12-18hrs feed, 8-12 hours water
o Pigs: feed 12hr, water 6-8hrs, hay/alfalfa/straw 2-3d

44
Q

Fasting: pigs

A

feed 12hr, water 6-8hrs, hay/alfalfa/straw 2-3d

45
Q

Fasting: Adult Horses

A

<4hr, 8-12hr - ??? NO CONSENSUS IN LJ
 Increases acidity, viscosity of gastric contents, may lead to enhanced risk of acidic fluid aspiration
 Typically browse for food, prolonged fasting can cause stress and individual horses and negatively influence motility of git or potentiate ulcerations

46
Q

Fasting: Foals

A

Foals: no fast if nursing, consider 1-2 hours for older foals

47
Q

Gastroesophageal Reflux

A

Common in dogs, cats under GA: incidence 0 to 66% dogs, 14-33% cats
* Normally silent during ax, noticed only if regurg occurs

Incidence of regurg: 0.63-1.3% dogs, 0-2% of cats

48
Q

Regurgitation

A

passive expulsion of food, fluid from esophagus into mouth/ejected from mouth
o Incidence of visual regurgitation MUCH lower, only visually confirmed in 0.63% of cases
o <1% of time when GER identified in 16-17% of cases
o Greater risk ASA >3, abdominal/imaging px, long ax, larger size

49
Q

MOA GER

A

abnormally low LES pressure (LESP), increased frequency/duration of transient lower esophageal sphincter relaxations (TLSRs)

50
Q

TLSR

A

Transient lower esophageal sphincter relaxation
normal events that vent gas formed in stomach, follow ingestion of food

51
Q

Changes in LES Pressure Contributing to GER

A

Intragastric pressure > LESP  barrier pressure normally btw two is lost
 Barrier pressure = LES P – intragastric P
 Decreases LES or increases intragastric favors reflux

Contributions from intraabdominal, intrathoracic pressure - increases favor GER

52
Q

LES Function

A

Functional sphincter – tonically contracted state until stimulated to relax via relaxation of UES +/- waves of peristaltic ctx

Tonic contraction of circular muscles, oblique gastroesophageal angle (horses), crura of diaphragm

Primarily PSNS+, hormones
–Vagus: excitatory input increases m tone, inhibitory decreases tone
–Relaxation via NO
–Increased tone from increased intragastric pressure

53
Q

Substances that Decrease LES Tone

A

NO, nitrates
Vasoactive intestinal peptide
Nicotine
alpha adrenergic agonists
Dopamine
Cholecystokinin
Secretin
Calcitonin Gene-Related Peptide

54
Q

Substances that Increase LES Tone

A

PGE2
M2, M3 R Agonists
Gastrin
Substance P
a2 Agonists
PFGa

55
Q

Drugs that Decrease LES Tone

A

Inhalants, N2O
Anticholinergics
ACP
a2s
Benzos
Opioids
Injectables: propofol (high doses), alfax, ketamine, TP
alpha adrenergic agonists
Nitroprusside
Ca Channel Blockers
Aminophyllines
Residual NMB
Cisapride
Cricoid Pressure (pharyngeal stimulation)
Pregnancy, Obesity
Hiatal Hernia
LMA
Dorsal Recumbency, Changes in Recumbency

56
Q

Drugs that Increase LES Tone

A

ACh
Anticholinesterases
Metoclopramide/Domperidone
Succinylcholine
Pancuronium, Vecuronium
Edrophonium, neostigmine
Histamine
Antiacids

57
Q

Drugs that Have No Effect in LES Tone

A

N2O (debated in literature), dexmed, remifentanil, propofol, propranolol, metoprolol, atracurium, NMB reversal, H2B, cimetidine, ranitidine, PPIs

58
Q

pH constant with gastric acid reflux

59
Q

pH consistent with bile acid reflux

A

> 7.5 bile reflux

60
Q

Main RF for GER

A

large breeds, brachycephalics, pregnancy, GI dz; orthopedic, abdominal, airway, neurological surgery, imaging

Most cases of anesthesia-related GER develop within 30’ if induction

61
Q

Positioning Triggers for GER

A

 Trendelenburg during laparoscopic sx, Trendelenburg alone does not
 Dorsal recumbency
 Changes in positioning

62
Q

Trendelenberg vs Reverse Trendelenberg

A

trendelenberg = head tipped down

Reverse = head RAISED

63
Q

Suctioning

A

Suction– does not change esophageal pH alone

Follow with lavage using tap water until retrieved fluid clear (increases pH above 4), NaBicarb instillation (increase pH >6.0 for 1.5-3hr), +/- pantoprazole IV

64
Q

Prolonged Fasting Times

A

o Prolonged fasting times associated with increased risk of reflux, lower gastric pH in anesthetized dogs

65
Q

Aspiration

A

Aspiration of GI contents perioperatively following GER, vomiting, +/- regurg
o Potential to also occur during heavy sedation, impairment of normally protective airway reflexes

Extent of damage depends on volume, type of reflux aspirated

66
Q

Complications of Aspiration

A

hypoventilation, hypoxemia, pneumonitis, bacterial pneumonia, +/- CPA
o Aspiration can be silent
o Unexplained oxygen desaturation, tachypnea, dyspnea or irregular respiratory patterns, auscultable abnormalities, blanching of MM may be seen

67
Q

Which lung lobes most commonly affected by aspiration pneumonia?

A

Right middle
Right cranial
Left cranial

68
Q

What are the three phases of aspiration pneumonia?

A
  1. Immediate, direct toxic damage to epithelium
  2. Inflammatory Reaction
  3. Bacterial Invasion/Infiltration
69
Q

First Phase of Asp Pneumonia

A

Immediate: direct toxic damage to epithelium, depends on amount/acidity
 Atelectasis, decreased compliance, VQ mismatch, decreased oxygenation

70
Q

Second Phase Asp Pneumonia

A

4-6h: inflammatory reaction –> pneumonitis
 Lesion may resolve if not severe

71
Q

Third Phase of Asp Pneumonia

A

Fulminant aspiration pneumonia DT bacterial invasion of damaged tissue

72
Q

Treatment Asp Pneumonia

A

o Early recognition, intervention = paramount to limiting severity
o 100% oxygen, head down, suction, bronchodilator, IPPV
o Humans: prophylactic ABX not recommended – only when infection confirmed
 Bacterial colonization later in process
 Exception: patients with FBO, chronic antiacid therapy – potential for enteric organisms in reflux fluid

73
Q

Incidence Asp Pneumonia?

A

0.17% (0.04-0.26%)

74
Q

Factors Assoc with AP - patient

A

ME, preexisting resp/neurologic dz
 IVDD: significant risk factors for AP included preanesthetic tetraparesis, cervical lesion, longer duration of anesthesia, PONV/regurg

75
Q

Factors Assoc with AP - procedure

A

upper airway surgery, endoscopy, thoracotomy, laparotomy, neurosurgery

76
Q

Factors Assoc with AP - anesthetic events

A

Regurgitation during/after GA, hydromorphone IV at induction

Boards: GI (4 decks)

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