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VET433B > Week 2 - GI > Flashcards

Week 2 - GI Flashcards

1
Q

What does dyspahgia mean?

A

a SYMPTOM (not a diagnosis) - difficult/abnormal swallowing

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2
Q

What are the two classification of dysphagia?

A
  1. Oropharyngeal
    -Oral
    -Pharyngeal
    -Cricopharyngeal (muscle related to upper esophageal sphincter/UES)
  2. Esophageal - delayed
    -exaggerated swallowing
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3
Q

Being a brachy sucks – why are they predisposed to dysphagia?

A
  1. stenotic nares
  2. elongated soft palate
  3. hypoplastic trachea
  4. inverted laryngeal sacules
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4
Q

How do brachycephalics get hiatal hernia?

A

bc they have a short muzzle > they have a mechanical obstruction in the upper airway (inspiratory stridor) > creates an increased negative intrathoracic pressure > this causes stomach to be sucked into chest cavity > weakness to diaphragm > hiatal hernia

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5
Q

When looking into dysphagia, which chem value should you look at?

A

CK!

and increased CK is not with Myasthenia Gravis

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6
Q

What is dysphonia?

A

-trouble talking/barking/meowing

caused by
neuropathy, junctionopathy, myopathy

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7
Q

How does anesthesia affect phagia?

A

-weakens LES tone (reflux can happen more easily)
-lose swallow reflex

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8
Q

What’s the difference between a video fluoroscopy and esophogram?

A

Esophogram
-giving contrast/barium by mouth – then taking radiograph right after
-2D dimensional image of esophagus
-document evidence of mechanical/anatomical defect in pharynx/esophagus
-single time point – can’t assess dynamics/motility

Video Fluoroscopy
-can assess dynamics/motility
-timing and opening of UES and LES
-can assess primary and secondary peristalsis
-assess reflux
-can assess everything from esophogram

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9
Q

What’s the Diagnostic Approach to the Dysphagic Dog?

A
  1. CT, MRI
  2. Electrodiagnostics (EMG, NCV) - helps with optimizing which muscle to biopsy
  3. Muscle biopsy
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10
Q

What are the muscles of mastication?

A
  1. pterygoid
  2. temporalis
  3. masseter
  4. digastric
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11
Q

What is MMM?

A

Masticatory Muscle Myositis

-autoimmune disease - dog’s immune system identifies the dog’s own muscle tissue as foreign and attacks it

-Inability to open the jaw under GA is a classical finding

-Usually bilateral

-Dobermans, Labradors, GSD, Rottweilers, Siberian husky, CKCS

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12
Q

What are some ways to DIAGNOSE MMM?

A

-CK may or may not be elevated! (acute yes, but could be normal if chronic)

-Serological assays: 2M antibody (ELISA)
–negative 2M doesn’t rule out MMM

-immunocytochemistry - false negatives if given corticosteroids within week

-Muscle biopsy - helps with diagnosis & long-term prognosis

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13
Q

What are the 2 types of Cricopharyngeal Muscle Dysphagia?

A
  1. Achalasia - Failure of cricopharyngeal muscle (CPm) to completely relax or open
    -Idiopathic hypertrophy of the CPm
    -there can also be LES Achalasia (achalasia is not sphincter specific)
  2. Asynchrony - Inappropriate timing in opening of UES
    -Idiopathic - thought to be a neuropathy
    -UES does open, just at the wrong time
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14
Q

What are CS of Cricopharyngeal Muscle Dysphagia?

A

-Dysphagia within seconds of swallowing
-Repeated swallowing attempts
-Dysphagia usually worse with water
-Nasal reflux
-Coughing
-Bloating

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15
Q

What is the opening to the UES?

A

Cricopharyngeal bar

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16
Q

How do you TREAT Cricopharyngeal Muscle Dysphagia?

A
  1. open surgical myotomy - PREFERRED
    -take out entire cricopharyngeal
  2. Closed CO2 laser myotomy
    -expensive, need special equipment
  3. Botox injection of CP muscle - temp
    -Botox causes temporary weakness of the CP muscle
    -15 Units injected in 3 sites directly in the CP muscle
    -Application of Botulinum Toxin
  4. Balloon dilation of UES - temp
  5. Enteral feeding device - temp
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17
Q

What is Megaesophagus?

A

generalized loss of motor function to the esophagus results in dilation and loss of normal peristaltic motility. result - food and fluid accumulate in esophagus

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18
Q

Myasthenia Gravis is seen in ____% of all Megaesophagus cases

A

25%

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19
Q

Esophageal Achalasia occurs in about ___% of dogs with Megaesophagus

A

70%

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20
Q

Megaesophagus can be congenital/primary (idiopathic) OR acquired form: primary (idiopathic) or secondary to underlying disease

A

Congenital/Primary Idiopathic ME: puppies at weaning

Acquired/Primary Idiopathic or Secondary to underlying dz: myasthenia graves, SLE, polymyositis, polymyopathies, dermatomyositis, Addison’s. Esophageal obstructive diseases, if they’re chronic enough.

Acquired idiopathic of ME is most common in dog - German shepherd, Great Dane, Irish Setter

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21
Q

In terms of congenital megaesophagus…

A

-Never see focal megaesophagus alone with congenital myasthenia gravis

-will see focal MEGAESOPHAGUS + systemic weakness in a young puppy with MYASTHENIA GRAVIS

-will commonly see puppies with CONGENITAL MEGAESOPHAGUS without MYASTHENIA GRAVIS

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22
Q

There is 2 forms of Myasthenia Gravis

A
  1. Congenital - rare, NOT AUTOIMMUNE
    -no need to draw blood for testing for antibodies bc not autoimmune
  2. Acquired - autoimmune
    -40% of cases only have focal ME without systemic weakness
    -45% of cases have severe ME with systemic weakness
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23
Q

How can you DIAGNOSE Myasthenia Gravis?

A
  1. Acetylcholine Receptor Antibodies – if suspecting autoimmune MG
    -normal is <0.6
    -may be normal still if acute onset
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24
Q

How do you MANAGE Idiopathic Megaesophagus?

A
  1. Modify consistency of the diet and water
  2. Feed from elevated position
    -Bailey Chair
  3. Gastrostomy feeding tubes
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25
Q

How do you MEDICALLY MANAGE Esophageal Achalasia/Achalasia of LES?

A

Achalasia of LES > INCREASES LES tone

goal: drugs that will reduce tone of LES

Phosphodiesterases
-Sildenafil
-Botulinum toxin injection at LES

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26
Q

How do you SURGICALLY MANGE Esophageal Achalasia/Achalasia of LES?

A

goal: reduce tone of LES

  1. Heller myotomy of LES - open LES, decreases tone of LES
    -con: may decrease tone too much and cause reflux
  2. Fundoplication - to combat reflux, but can’t be too tight bc back at square one

DIS1-2, page 14

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27
Q

What does dysmotility mean?

A

foods and liquids do not easily pass down the esophagus

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28
Q

How was Coco’s Sliding hiatal herniation fixed? From DIS1-DIS2

A

3 surgeries

  1. gastropexy
  2. esophagopexy
  3. esophageal plication
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29
Q

What are the types of Hiatal Hernias?

A
  1. Type I Sliding Hiatal Hernia
    -LES is above the diaphragm in chest cavity
  2. Paraesophageal Hiatal Hernia

DIS1-2, page 16

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30
Q

What are the CAUSES of Esophagitis?

A
  1. Secondary to Anesthesia
    -7.5 days post-anesthesia
    -Presumed GER (incidence of gastroesophageal reflux under anesthesia is 16-55%)
  2. Pill-induced esophagitis
    -Doxycycline
    -Clindamycin
  3. Vomiting gastric contents
  4. Secondary to foreign body injury
  5. Secondary to ingestion of caustic material
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31
Q

When there is a decrease in tone/reduction in LES pressure, what can happen? This decrease is common under anesthesia.

A

GER - gastroesophageal reflux

-Morphine, atropine, acepromazine, thiopentol, xylazine, isoflurane
-Large-breed dogs (> 40kg; orthopedic surgery procedures)

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32
Q

How do you MANAGE esophagitis?

A
  1. Gastric acid suppressants
    -Proton pump inhibitors (omeprazole, pantoprazole, etc.)
    -H2-receptor antagonists (famotidine, ranitidine)
  2. Sucralfate

3.Prokinetics

Cisapride
Metoclopramide

  1. Dietary fat restriction (more relevant in dogs than cats)
  2. PEG tube?
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33
Q

How does Sucralfate work in managing Esophagitis?

A

*Sulfated sucrose + polyaluminum hydroxide
– Binds to proteins electrostatically
– Stimulates PG production
– Adsorption of bile salts
– Inactivation of pepsins

  • Adverse effects:
    – Constipation
    – Inhibit absorption of other drugs

works best in acidic environments, but usually given with PPIs – PPIs raise pH - make things more basic. So usually give sucralfate first, wait, and THEN PPI.

Sucralfate is a band-aid. Doesn’t truly fix issue.

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34
Q

How do PPIs and H2 blockers/antagonists work? Which is better?

A

PPI
-increase gastric pH, make more basic/less acidic. The H/K+ ATPase gets shut down, so not enough H to make acidic.
-better at suppressing acid
-not subject to tolerance

H2 blockers/antagonists
-block basal level of gastric acid secretion by binding to histamine type 2 receptors = decrease gastric acid production
-only works for a few days

when giving to these drugs – usually at least BID, then taper when need to discontinue (no cold turkey)

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35
Q

How does Cisapride work in managing Esophagitis?

A

-increases LES tone

-Stimulates gastric emptying

-Stimulates distal esophageal motility in cats, humans, guinea pigs
–Gastroesophageal reflux
–Esophagitis

CONTRAINDICATED in dogs with megaesophagus (dogs with ME already have increased tone of LES)
-also don’t give metaclopramide

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36
Q

Metaclopramide can be used for colonic motility. T/F

A

FALSE, cisapride helps with small intestine and colonic motility – NOT metaclopramide

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37
Q

What is vomiting?

A

-Forceful expulsion of gastrointestinal contents

-Active abdominal contractions

-Neurologically-mediated reflex

-retching and salivation

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38
Q

There are GI and Extra GI causes to vomiting. What are some examples?

A

GI
– Dietary indiscretion
– GI foreign body
– GI neoplasia
– Pancreatitis (Can also be extra GI)
– Infectious gastroenteropathy
– IBD

Extra GI
– Liver disease
– Renal disease
– Hyperthyroidism
– Toxin exposure
– Addison’s
– Heartworms
– Vestibular

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39
Q

What disease can cause chronic vomiting in cats?

A

Chronic small bowel disease is a common cause

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40
Q

What are the top 3 GI neoplasia in the cat?

A
  1. Lymphoma - small cell lymphoma (T cells)
  2. mast cell
  3. adenocarcinoma (most common gastric neoplasia in dog)
41
Q

The Vomiting Reflex involves which two pathways?

A
  1. Humoral pathway (Bloodborne) - CRTZ (chemoreceptor trigger zone)
    -blood-borne substances that affect the CRTZ
  2. Neural pathway – Vomiting Center
    -influenced by inflammation, infection, malignancy or toxicity of the GI tract that result in activation of the emetic center

things like chemotherapy drugs or severe renal dz can trigger both pathways

42
Q

What are the 4 components of the Vomiting Reflex?

A
  1. Visceral receptors in GI tract, peritoneum, bile ducts
  2. Vagal and sympathetic afferent neurons
  3. CRTZ
  4. Vomiting center
43
Q

Histaminergic neurons and the CRTZ are
involved in motion sickness (vestibular nuclei) in the dog or cat?

A

Histaminergic neurons and the CRTZ are involved in motion sickness in the DOG

-H1-receptor antagonists work well in the
dog for preventing or managing motion sickness, but not in the cat.

-ex of Histaminic drug - Benadryl

44
Q

Motion sickness (vestibular nuclei) in cats is thought to be influenced by receptors in the __________, which is why ____________ would be a better choice for managing motion sickness.

A

-vomiting/emetic center

-α2-receptor antagonists

45
Q

D2 dopamine receptor AGONIST is a potent emetic agent in the dog or cat? D2 dopamine receptors found at CRTZ

A

DOG

ex. of D2 dopamine AGONIST – Apomorphine

1) CRTZ D2 dopamine receptors are not as important in mediating humoral emesis in the cat

2) D2 dopamine receptor antagonist (e.g., metoclopramide (Reglan)) is a relatively ineffective anti-emetic agent in the cat.

46
Q

5-HT3 receptor ANTAGONISTS are effective for the prevention of emesis associated with chemotherapy in dogs or cats?

A

BOTH, effective in dogs and cats

5-HTC receptors found at:
Vomiting center
CRTZ
Pharynx and GIT

Antagonist 5-HT3 drugs: Dolasetron (Anzemet) and ondansetron (Zofran)

47
Q

What are the differences between REGURGITATION and VOMITING?

A

REGURGITATION
* Passive – typically no abdominal contractions
* No prodromal nausea
* Seconds to hours after meal (hours post meal is class for ME)
* Usually undigested material in evacuated contents

VOMITING
* Active – abdominal contractions
* Prodromal nausea
* Minutes to hours after meal
* Undigested or digested material in evacuated contents ± bile

48
Q

What’s the approach to a vomiting dog?

A
  1. Determine whether animal is vomiting, regurgitating, retching,
    or coughing
  2. Determine if animal has mild, self-limiting or more serious problem
    – History
    – Physical exam
    – Minimum data base
    – Clinical experience
  3. Determine if vomiting is due to primary GI or extra-GI disease
    -History
    -Physical exam
    -Chemistry panel
    -Serum T4
    -Abdominal imaging
49
Q

What are signs of SERIOUS DISEASE in vomiting animals?

A
  • Fever
  • Melena or hematochezia
  • Weakness
  • Anorexia > 48 hrs
  • Abdominal pain
  • Vomiting of “coffee grounds” or frank blood (hematemesis)
  • Pale, icteric or muddy mucous membranes
  • Enlargement of abdominal organs/peripheral Ln’s
50
Q

What are some important history points with a vomiting animal?

A
  • Vaccination status
  • Deworming history
  • Travel history
  • Dietary changes
  • Previous medical problems
  • Physical characteristics of vomitus
  • Relationship of vomiting episodes to meals
51
Q

Patients with polymyositis test negative for antibodies against type 2M fibers. How do you DIAGNOSE Polymyositis?

A

A MUSCLE BIOPSY is necessary to confirm a diagnosis of polymyositis and helps determine prognosis

52
Q

How do you treat MMM?

A

immunosuppression

by corticosteroid or cyclosporine administration

53
Q

What are practical diagnostic testing for ACUTELY vomiting patients?

A
  • PCV/TP
  • Glucose - Diabetic ketoacidosis
  • Azostix - kidney function
  • Urine SG - kidney function
  • Abdominal radiographs - foreign bodies
  • ± Zinc sulfate fecal flotation - pup/kits parasites
  • ± Resting cortisol - Addison’s
54
Q

How do you MANAGE an acute vomiting patient?

A

DO
* Crystalloid fluid administration
-hydration will allow maintenance of gastric mucosal blood flow
* Dietary management (bland diet)
-only feed if NOT vomiting intractably – bc then at risk for aspiration
-for dogs, feed low fat — high fat can increase GI emptying
* Antiemetics
* Broad spectrum anthelminthic - get rid of parasites!

DON’T
* NPO
- little benefit to withholding food and water in an effort to “rest” the GI tract
* Gastric acid suppressants
* Antibiotics
-should be avoided unless the patient is febrile, or has evidence of hematemesis or bloody diarrhea suggesting breakdown of the gastrointestinal mucosal barrier
*Corticosteroids

55
Q

What are practical diagnostic testing for CHRONICALLY vomiting patients?

A
  1. Complete blood count
  2. Serum chemistry profile
  3. Urinalysis
  4. Fecal flotation
  5. Serum T4 (cats)
  6. Serum B12/folate - check for EPI
  7. FeLV/FIV (cats)
  8. Abdominal ultrasound and/or radiographs
  9. Resting cortisol and/or ACTH stimulation test
56
Q

Diagnostic Approach to the Chronically Vomiting Dog and Cat

A
  • Contrast radiography
    – Gastrogram -not really done bc everything can just be seen on US
    – Upper GI series
  • Serum bile acids
  • Serum Spec cPL or fPL
  • Liver aspirate or biopsy
  • GI biopsies
57
Q

What’s the value of a Chem panel for the Vomiting Dog and Cat?

A
  • Renal disease
  • Diabetic ketoacidosis (should not be vomiting if only diabetic)
  • Liver disease
  • Hypercalcemia
  • Electrolyte abnormalities (Na and K+)
  • Hyperthyroidism (not on standard panel)

!!!Addison’s cannot be r/o on basis of normal electrolytes! (Atypical Addison’s)

58
Q

What can be ruled out on a chem panel?

A
  • Renal disease
  • Diabetic ketoacidosis
  • Liver disease
  • Hypercalcemia

NOT addison’s, not hyperthyroidism

59
Q

Can you get full thickness biopsies with endoscopy?

A

No

limitation of endoscope - working length, might not get far enough

60
Q

What is Gastritis?

A

Gastritis is a non-specific term reflecting inflammation of the
stomach – it can have many different causes including IBD, foreign body, toxin ingestion, infections, etc.

presence of chronic inflammatory changes within
the gastric mucosa in conjunction with clinical signs of gastritis

61
Q

What is IBD? Inflammatory Bowel Disease

A

IBD refers to a group of idiopathic chronic GI disorders
characterized by infiltration of the GI tract with inflammatory cells

IBD can cause gastritis

IBD can affect the stomach, small bowel, or colon

62
Q

What are 2 common histologic subtypes of infiltration with IBD?

A

EOSINOPHILIC GASTRITIS and LYMPHOCYTIC-PLASMACYTIC GASTRITIS

are two of the more common histologic subtypes of infiltration
associated with inflammatory bowel disease (IBD) of the stomach or intestine

treated w pred

63
Q

Importance of Helicobacter spp. Infection in gastritis?

A
  • Helicobacter spp. have been frequently identified in gastric
    biopsies from healthy dogs and cats - causes chronic inflammation to lining of stomach
    – Role of Helicobacter in dogs and cats is still unclear
    – Lymphofollicular gastritis on histo
    – Triple therapy can be used to manage patients
  • Metronidazole, ampicillin, bismuth subsalicylate
  • Clarithromycin, metronidazole, PPI
64
Q

What are examples of GI protectants?

A
  • Diffusion Barriers
    – Sucralfate
  • H2-blockers/H2 receptor antagonists
    – Famotidine, Ranitidine
  • H+K+ ATPase Inhibitors (PPIs)
    – Omeprazole, Esomeprazole, Pantoprazole
  • Prostaglandin E1 Analogues
    – Misoprostol
65
Q

Sucralfate is a diffusion barrier. How does it help? Remember, it also helps with esophagitis.

A

-sustained local protective effect against acid, pepsin and bile at the ulcer site, forming a protective barrier.

-sucralfate increases the luminal concentration of prostaglandin E2 which is also protective against ulcerogenic factors.

-not absorbed from the gastrointestinal tract, it has virtually no systemic toxicity

-may also inhibit the absorption of other drugs

66
Q

H2 receptor antagnists and H/K ATPase inhibitors are GI protects that suppress acid. How do they work?

A

H2-receptor antagonist agents competitively block the H2 receptor on the parietal cell, reducing gastric acid secretion

PPIs (like Omeprazole) irreversibly blocks the gastric proton pump (hydrogen-potassium ATPase), causing a
marked decrease in gastric acid secretion

H2 receptor antagonists are not as effective/potent as PPIs (H/K ATPase inhibitors)

PPIs should be given at a dose of 1mg/kg q12 hours and should be given 30-60 min before meals

PPIs should be tapered before discontinuation - to avoid hyper secretion acid rebound

67
Q

Misoprostol is a GI protectant – it is a Prostaglandin E1 Analogues. How does it work?

A

indicated for non-steroidal ulcers, don’t use for if it not a non-steroidal (like NSAIDs = non steroidal) ulcer

  • Stimulates mucosal blood flow
  • Decreases gastric acid secretion
  • Increase mucus
  • Increase epithelial cell turnover
  • Increasing bicarbonate and mucus secretion
  • Inhibiting back diffusion of hydrogen ions
  • Enhancing mucosal blood flow
  • Preserving mucosal regenerative capacity

DON’T USE IN ANIMAL IF IT’S NOT A NON-STEROIDAL ULCER

use for ulcers caused by NSAIDs

68
Q

When would you use an antiemetic?

A
  • Vomiting is intractable
  • Risk of aspiration pneumonia
  • Onset of acid-base or electrolyte disorders
    – No evidence of obstruction or toxin
    – Client does not desire definitive diagnosis
69
Q

What is Reglan (Metoclopramide)? Antiemetic

A
  • Antiemetic (D2-dopaminergic antagonistic activity, and weak 5-HT3 antagonistic activity) and prokinetic drug (could exacerbate diarrhea)
  • Prokinetic activity is far weaker vs. cisapride
  • Relatively ineffective drug for vomiting cats
  • Does NOT work on the COLON
  • Very short half-life: best given as a CRI
    – 1-2 mg/kg/24 hr
70
Q

What is Zofran (Ondansetron)? Antiemetic

A
  • Very potent antiemetic in dogs and cats
  • 5HT3-receptor antagonist
  • Can be given IV or SQ
  • SQ more effective in cats
  • 0.5-1.0 mg/kg q12-24h

-no prokinetic activity

71
Q

What are some ɑ-2 Adrenergic Antagonists? Antiemetics

A

– Chlorpromazine (used for motion sickness in cat)
– Prochlorperazine

– Yohimbine
-not effective alone

72
Q

What are examples of Anticholinergic drugs? aka antimuscarinic drugs, parasympatholytics

A

Atropine
Glycopyrrolate

73
Q

Why should we use Anticholinergics with anesthesia? How does it help with patients with GI disease?

A
  1. prevention or treatment of sinus bradycardia, 1st and 2nd degree AV block due to increased vagal tone
  2. reduction of secretions (respiratory, GI)

MAIN GI effects:
* Reduced secretions (saliva, gastric, intestinal)
* Decreased GI motility
* Decreased lower esophageal sphincter tone
* Increased gastric pH

74
Q

What a H2-blocker/antagonist example?

A

Famotidine

75
Q

How does H2-blocker/antagonists (like Famotidine) help with patients with GI disease? How does it help under anesthesia?

A
  • Decrease gastric (acid) secretions
  • Increase gastric pH
  • In anesthesia, used (with H1 blockers) in patients with mast cell tumors
76
Q

PPIs – proton pump inhibitors – what’s an example?

A
  • Pantoprazole (omeprazole, esomeprazole)
77
Q

How do PPIs work?

A
  • Irreversible inhibition of H+/K+-ATPase
  • Decrease gastric (acid) secretion
  • Increase gastric pH
78
Q

Why use a PPI in anesthesia?

A
  • Prevention of esophagitis in patients at risk of gastroesophageal reflux or regurgitation
  • Decreased severity of aspiration pneumonia
79
Q

What an example of a common antiemetic?

A

Maropitant/Cerenia

  • NK1 receptor antagonist - events substance P to bind to NK1
  • Reduces opioid-induced emesis
  • If administered prior to opioid
  • Reduces anesthetic requirements
  • May not reduce post-operative nausea and vomiting
  • Most common antiemetic used for anesthetized patients
    *works at GI tract, CRTZ, and committing center
80
Q

What are examples of opioids?

A
  • Hydromorphone, oxymorphone, morphine, methadone, meperidine, fentanyl, butorphanol, buprenorphine
81
Q

What are GI effects of opioids?

A
  • Reduce GI motility/increase transit time
  • Vomiting (mostly full μ-agonists, effect on CTRZ) - initial dose
  • Antiemetic (mostly full μ-agonists, effect on vomiting center) - repeated doses
  • Decreased lower esophageal sphincter tone/
    increased risk of regurgitation
82
Q

Acepromazine is a Phenothiazine. What are its GI effects?

A
  • Antiemetic
  • Delays gastric emptying
  • Decreases GI motility/increases transit time
  • Decreases lower esophageal sphincter tone/increases risk for regurgitation
83
Q

What an example of an a2-agonist?

A

Dexmedetomidine, medetomidine, xylazine,
romifidine

84
Q

What are GI effects of a2-agonists?

A
  • Vomiting (cats > dogs)
  • Decrease lower esophageal sphincter tone/increase risk of regurgitation
  • Decrease intestinal motility
85
Q

What are some examples of benzodiazepines?

A
  • Midazolam, diazepam, zolazepam
86
Q

What GI effects do benzodiazepines have?

A
  • Decrease lower esophageal sphincter tone/
    increase risk of regurgitation
87
Q

What are the main GI effects of Propofol?

A
  • Antiemetic (subanesthetic doses? Well demonstrated in humans)
  • Decrease gastric emptying
  • Decrease intestinal motility
88
Q

What are the main GI effects of Alfaxalone?

A
  • Largely unknown
  • Decreases lower esophageal sphincter tone
89
Q

What are the main GI effects of Ketamine?

A
  • Decrease intestinal motility at high dose
  • Low doses are expected to have minimal effects
90
Q

What are the main GI effects of inhalants? Iso/Sevo

A
  • Decreased lower esophageal sphincter tone/increase risk of regurgitation
  • Decreased gastrointestinal motility

SEE Lecture 5 Slide 16

91
Q

What are factors that contribute to gastro-esophageal reflux?

A

– Increasing age

– Abdominal procedure

– Longer fasting time
* Recommendation for optimal fasting?

– Drugs
* Phenothiazine/atropine > diazepam
* Morphine > meperidine, acepromazine

  • Factors without impact
    – Position
    – Isoflurane vs halothane vs sevoflurane
  • Factors decreasing incidence
    – High dose metoclopramide (bolus + CRI)
    – Cisapride
92
Q

Why would rapid sequence induction be indicated? What drugs can be used?

A
  • Indicated whenever a rapid control of the airway is required
  • In patients at risk for vomiting-regurgitation
    – Full stomach (postpone if elective)
    – Megaesophagus
    – Intestinal obstruction
  • Drugs
    – Propofol
    – Ketamine
    – Alfaxalone
    – Etomidate
  • Contraindicated
    – Inhalants
    – Opioids
93
Q

What are complications of Vomiting, regurgitation, gastro-
esophageal reflux?

A
  1. Esophagitis
  2. Aspiration pneumonia
    * Incidence 0.17%?
    * Severity depends on pH, particulate matter in aspirated
    material
    * Crackles and wheezes in dependent lung lobes
    * Hypoxemia
94
Q

What are some risk factors for Aspiration Pneumonia?

A
  • Hydromorphone
  • Regurgitation
  • Surgery
    -Laparotomy
    -Upper airway surgery
    -Neurosurgery
    -Thoracotomy
  • Endoscopy
  • Megaesophagus
  • History of neurologic disease
  • History of respiratory disease
95
Q

What are the goals of anesthesia for a patient with GI dz?

A
  • Avoid exacerbation of primary problem
  • Prevent vomiting/regurgitation/reflux if possible
  • Prevent adverse effects (esophagitis, pneumonia) if they occur
  • Correct dehydration/hypovolemia and
    electrolyte and acid-base imbalances
  • Provide adequate procedural conditions
  • Prevent post-operative ileus
96
Q

How do you PREVENT ileus? in human

A
  • Maintain intestinal oxygenation and blood flow
    -Goal oriented fluid therapy
    -Avoid fluid overload
    -Avoid/treat hypotension
    -Avoid/treat low blood oxygenation
  • Provide good analgesia
  • Decrease opioids
    -Local/regional anesthesia
    -NSAIDs (caution with GI disease)
    -Epidural morphine
    -Intravenous lidocaine
    –Prokinetic???
    –Antiinflammatory
  • Surgical technique
  • Minimize handling of intestines
  • Laparoscopy
    -Preferred to laparotomy
    -Abdominal insufflation with helium better than CO2 better than air
97
Q

What is post-op care for ileus?

A
  • Enteral nutrition and ambulation ASAP
  • Prevent constipation
  • Peripheral opioid antagonists
    (methylnaltrexone)
  • Prokinetics (e.g. cisapride)
98
Q

What are some anticipated problems related to anesthesia?

A
  • Problems caused by anesthesia (i.e. by the anesthesia
    state and by the drugs used to produce this state)
  • Hypotension
  • Hypoventilation
  • Hypothermia
  • (Bradycardia)
  • ± problems specific to some drugs (e.g. myoclonus with
    etomidate)
99
Q

What are some anticipated problem related to the procedure? How about the disease?

A
  • Procedure related
  • Directly related to the procedure
  • Examples: pain, bleeding (surgery), stomach
    distention (gastroscopy)
  • Disease related
  • Caused by the disease process
  • Examples: vomiting, regurgitation, electrolyte
    imbalances

VET433B (8 decks)

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