Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Boards: GI > GI Physiology > Flashcards

GI Physiology Flashcards

1
Q

Monogastric Species

A

Dogs, Cats, Pigs (spiral colon)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Ingesta Travel through Ruminants

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Gas Production in Sheep

A

5L/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Gas Production in Cattle

A

30L/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

UES

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

LES

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Esophageal M composition - dogs

A

striated m

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Esophageal M composition - other species

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Camelids

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Enteric NS

A
  1. Extrinsic components
  2. Intrinsic = myenteric, submucosal plexuses (SMP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Myenteric Plexus

A

btw circular, longitudinal m layers – controls intestinal motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Submucosal Plexus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Extrinsic ENS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Two Patterns of Muscular Activity with GIT

A
  1. Migrating Motor Complexes (MMCs)
  2. Digestive pattern when food enters stomach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cats and MMCs

A

migrating spike complex, weaker than MMC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Effect of Nervous System on GI Motility

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Changes in GIT Assoc with Pregnancy
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
26
Effects of Ax on GIT Function
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
27
Most significant perianesthetic GIT complication?
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
28
Which NT stimulate vomiting?
Serotonin (5HT, 5HT3), histamine, ACh, dopamine, neurokinin 1 (NK-1), substance P
29
Other Stimulations for vomiting
cerebral cortex (anxiety, anticipation), vestibular apparatus (motion sickness), local damage to/distension of GIT via release of serotonin or stimulation of vagal afferent neurons
30
CRTZ
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
31
Area Postrema
**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
Vestibular System
within temporal lobe Changes in equilibrium, CN 8 afferents via H1/muscarinic AChR to vomiting center
33
Cortex
Anticipatory/anxiety-induced vomiting originates in cerebral cortex Also increased ICP, meningial irritation Via GABA, H1
34
Communication from GIT
Enterochromaffin cells in GIT release serotonin >> 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
Stretch, mechano R in GI
 Mechanoreceptors in pharynx + Tension receptors / Chemoreceptors in stomach, duodenum >> stimulation sends signals to VC in BS * GOAL: noxious tactile or chemical stimulation in GI mucosa results in clearance of offending stimulus
36
Three Phases of Vomiting
1. Projection Phase 2. Retching Phase 3. Ejection Phase
37
Projection Phase
* Nausea, reverse peristalsis of SI --> pushes proximal small bowel contents back into stomach * Secretion of saliva via PNS, tachycardia via SNS
38
Retching Phase
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
Ejection Phase
* 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
Fasting: Adult SA
: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
Fasting: Pediatric SA
<8wk, <2kg: no longer than 1-2hr
42
Fasting: Adult Bovids
feed 24-48hr, water 6-12hr
43
Fasting: calves, SR, camelids
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
Fasting: pigs
feed 12hr, water 6-8hrs, hay/alfalfa/straw 2-3d
45
Fasting: Adult Horses
<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
Fasting: Foals
Foals: no fast if nursing, consider 1-2 hours for older foals
47
Gastroesophageal Reflux
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
Regurgitation
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
MOA GER
abnormally low LES pressure (LESP), increased frequency/duration of transient lower esophageal sphincter relaxations (TLSRs)
50
TLSR
Transient lower esophageal sphincter relaxation normal events that vent gas formed in stomach, follow ingestion of food
51
Changes in LES Pressure Contributing to GER
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
LES Function
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
Substances that Decrease LES Tone
NO, nitrates Vasoactive intestinal peptide Nicotine alpha adrenergic agonists Dopamine Cholecystokinin Secretin Calcitonin Gene-Related Peptide
54
Substances that Increase LES Tone
PGE2 M2, M3 R Agonists Gastrin Substance P a2 Agonists PFGa
55
Drugs that Decrease LES Tone
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
Drugs that Increase LES Tone
ACh Anticholinesterases Metoclopramide/Domperidone Succinylcholine Pancuronium, Vecuronium Edrophonium, neostigmine Histamine Antiacids
57
Drugs that Have No Effect in LES Tone
N2O (debated in literature), dexmed, remifentanil, propofol, propranolol, metoprolol, atracurium, NMB reversal, H2B, cimetidine, ranitidine, PPIs
58
pH constant with gastric acid reflux
<4.0
59
pH consistent with bile acid reflux
>7.5 bile reflux
60
Main RF for GER
large breeds, brachycephalics, pregnancy, GI dz; orthopedic, abdominal, airway, neurological surgery, imaging Most cases of anesthesia-related GER develop within 30' if induction
61
Positioning Triggers for GER
 Trendelenburg during laparoscopic sx, Trendelenburg alone does not  Dorsal recumbency  Changes in positioning
62
Trendelenberg vs Reverse Trendelenberg
trendelenberg = head tipped down Reverse = head RAISED
63
Suctioning
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
Prolonged Fasting Times
o Prolonged fasting times associated with increased risk of reflux, lower gastric pH in anesthetized dogs
65
Aspiration
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
Complications of Aspiration
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
Which lung lobes most commonly affected by aspiration pneumonia?
Right middle Right cranial Left cranial
68
What are the three phases of aspiration pneumonia?
1. Immediate, direct toxic damage to epithelium 2. Inflammatory Reaction 3. Bacterial Invasion/Infiltration
69
First Phase of Asp Pneumonia
Immediate: direct toxic damage to epithelium, depends on amount/acidity  Atelectasis, decreased compliance, VQ mismatch, decreased oxygenation
70
Second Phase Asp Pneumonia
4-6h: inflammatory reaction --> pneumonitis  Lesion may resolve if not severe
71
Third Phase of Asp Pneumonia
Fulminant aspiration pneumonia DT bacterial invasion of damaged tissue
72
Treatment Asp Pneumonia
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
Incidence Asp Pneumonia?
0.17% (0.04-0.26%)
74
Factors Assoc with AP - patient
ME, preexisting resp/neurologic dz  IVDD: significant risk factors for AP included preanesthetic tetraparesis, cervical lesion, longer duration of anesthesia, PONV/regurg
75
Factors Assoc with AP - procedure
upper airway surgery, endoscopy, thoracotomy, laparotomy, neurosurgery
76
Factors Assoc with AP - anesthetic events
Regurgitation during/after GA, hydromorphone IV at induction

Boards: GI (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions