Vomiting and regurgitation Flashcards

1
Q

List differencces between regurgitaiton and vomiting

A

Clinical sign

Regurgitation

Vomiting

Nausea or salivation

No

Common

Retching (abdominal contractions)

No

Common

Presence of bile

Rare

+/-

Cervical oesophageal distension

+/-

No

Amount of material

Any

Any

Time after eating

Variable

Variable

pH (poor indicator)

Variable – usually neutral high

Variable – usually low pH

Prodromal signs (salivation/lip smacking)

sometimes

often

Material expelled when head lowered

Typically

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2
Q

Explain the pathophysiology of regurgitation

A
  • Dogs: the oesophageal body is completely striated muscles
  • Cats: distal 1/3 to ½ of oesophagus is smooth muscle
  • In both species during swallowing the upper oesophageal sphincter relaxes to allow passage of food or liquid into the proximal oesophagus
  • A primary peristaltic wave is moved distally to the stomach.
  • Secondary peristaltic waves are generated in response to intraluminal distension to clear remaining material.
  • Lower esophageal sphincter relaxes as food approaches as passes into somach.
  • Diseases resulting in inflammation, obstruction, or hypomotility in oesophagus interrupt the normal process causing regurgitation.
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3
Q

Explain the differentials and diagnosis of regurgitation

A
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4
Q

Explain vomiting

A
  • Active expulsion of ingesta from stomach and sometimes duodenum through the mouth.
  • Vomiting involves centrally mediated reflex with coordinated closure of the nasopharynx and glottis to protect the airway reducing risk of aspiration pneumonia
  • Vomiting evolved to protectagainst ingestion oftoxic or noxious substances which explaines activating neural and humoral stimli
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5
Q

Explain the pathophysiology of vomiting

A
  • Initiated by emetic center composed of nuclei in medulla oblongata in the brainstem.
  • Neurokinergic (NK1) receptors located in the adjacent nucleus tractus solitary (NTS) -> stimulates the emetic center.
  • Activation of receptors may occur indirectly by humoral pathways via chemoreceptor trigger zone (CRTZ) or directly through neural pathways from the GI tract, cerebral cortex, or vestibular system.
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6
Q

Complete the diargram

A
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7
Q

Where is the Central trigger zone located? How does it sample blood

A

CRTZ located in area postrema in fourth ventricle floor lacks BBB -> allowing sampling of chemical stimuli in the blood.

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8
Q

What receptors does the central trigger zone have?

A

CRTZ has dopimanergic (D2), histaminergic (H1), adrenergic (alpha2), serotonergic (5HT3), cholinergic (M1), enkephalinergic (ENK ), and neurokinergic (NK1) receptors.

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9
Q

Why doesnt apomorphine work in cats?

A
  • Apomorphine (D2 and D2 agonists) is potent stimulator of emesis in dogs but has little to no effect in cats, suggesting lack of D2 receptors in species.
  • Xylazine is effective emetic in cats suggesting that alpha2 receptors may be important
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10
Q

What pathways are involved in neural stimulation of vomiting?

A
  • Neural stimulation occurs via afferent vagal, sympathetic, vestibular, and cerebrocortical pathways.
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11
Q

How does GIT disease stimulate vomiting?

A
  • GIT disease directly causes vomiting by stimulating release of serotonin from enterochromaffin cells that bind 5HT3 receptors on afferent vagus nerves (dog or the CRTZ (cat)
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12
Q

What is the appropriate clinical approach to a vomiting patient?

A

Description of vomiting episodes to differentiate from coughing or regurgitation

  1. frequency, duration, relation to eating or drinking, and vomitus
    1. >8hrs after ingestion-> suggests delayed gastric emptying due to gastric outflow obstruction or hypomotility
    2. bile suggests patency of gastric outflow tract
    3. Fresh or digested blood indicates GI erosions or ulcers
  2. Acute or chronic (>1-2 weeks) or sporadic (intermittent acute)

Dietary history

  1. Past, and current diets
    1. Changes or opening a new bag, or can of food
  2. Medication: drugs, supplements, nutraceuticals, and alternative herapies
  3. Exposure to toxin or foreign body
  4. Vaccination status, travel history, exposure to other animals

Physical exam

  1. Patient demeanor
  2. Oral exam
    1. ulcers associates with uremia or toxins
    2. lingual linear foreign body
    3. icteric MM -> liver disease
  3. Cardiac arrhythmia -> metabolic derangements or toxin ingestion
  4. Abdomen palpation for
    1. Pain -> pancreatitis, obstruction
    2. Effusion -> peritonitis
    3. Gas distension -> obstruction, gastric dilation-volvulus,
    4. Organomegaly
  5. Rectal exam -> melena, constipation, or foreign body material
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13
Q

Outline your diagnostic approach to acute vomiting?

A
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14
Q

Outline your diagnostic approach to chronic vomiting

A
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15
Q

List the metabolic disease causes of vomiting?

A

Metabolic disease

Renal disease

Hepatobiliary disease or failure

Electrolyte derangements

Endotoxaemia

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16
Q

List the endocrine diseases causing vomiting

A

Endocrine

Hypoadrenocorticism

Hyperthryoidism

17
Q

List toxins/drugs that can cause vomiting

A

Toxins/Drugs

Heavy metals

Ethylene glycol

NSAIDs

Antibiotics

Chemotherapy agents

18
Q

List dietary causes of vomiting

A

Dietary Causes

Indiscretion

Allergy

Intolerance

19
Q

List abdominal disease causes of vomiting

A

Abdominal Disease

Pancreatitis

Peritonitis

Neoplasia

20
Q

List gastric causes of diseases

A

Gastric Diseases

Gastritis

Parasites

Helicobacter

Foreign body

Obstruction

GDV

Motility disorders

Neoplasia

21
Q

List small intestinal diseases that can cause of vomiting

A

SI disease

IBD

Neoplasia

Obstruction

Parasites

Infections

22
Q

List large intestinal diseases that can cause of vomiting

A

LI disease

Constipation

Colitis

23
Q

List antiemetic drugs, their site of action, and classification

A

Classification

Drugs

Sits of action

Dosages

Alpha2 antagonists

prochlorperazine

CRTZ, emetic center

0.1-0.5mg/kg SC, IM q 6-8h

chlorpromazine

CRTZ, emetic center

0.1-0.4 mg/kg SC q 8h

D2 antagonists

Metoclopramide

CRTZ, GI Smooh muscle

0.2-0.4 mg/kg SC, IM q 8h; 1-2 mg/kg/day CRI IV

Domperidone

CRTZ, GI smooth muscle

0.1-0.3 mg/kg IM, IV q 12h

Prochlorperazine

CRTZ, emetic center

0.2-0.5 mg/kg IM q 6-8h

Chlorpromazine

CRTZ, emetic center

0.2-0.4 mg/kg SC q 8h

5HT3 Antagonists

Ondansetron

CRTZ, vagal afferents

0.5-1 mg/kg PO IV q 12h

Dolasetron

CRTZ, vagal afferents

0.6-1 mg/kg PO, IV q 12h-24h

NK1 antagonists

Maropitant

CRTZ, emetic center

1mg/kg SC or IV q 24h; 2mg/kg PO q 24h

ENK

Butorphanol

CRTZ

0.2-0.4 mg/kg IM, SC q 12h

M1 antagonists

Prochlorperazine

CRTZ, emetic center

0.1-0.5 mg/kg SC, IM q6-8h

Chlorpromazine

CRTZ, emetic center

0.2-0.4 mg/kg SC q 8h

H1 antagonists

Diphenhydramine

CRTZ

2-4 mg/kg PO, IM q 8h

Prochlorperazine

CRTZ, emetic center

0.1-0.5 mg/kg SC, IM q 6-8h

Chlorpromazine

CRTZ, emetic center

0.2-0.4 mg/kg SC q 8h

24
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A