Vomiting Flashcards
VOMITING PHASES
Nausea Retching Expulsion
PHASE 1 – NAUSEA
Or … Prodromal Phase Clinical Signs
Ptyalism
Hiding
Seeking attention
Yawning
Shivering Tachycardia Pallor
PHASE 2 - RETCHING
Abdominal muscles, chest wall and diaphragm all contract without any expulsion of gastric contents
Retrograde contractionduodenal contents into stomach
Deep inspiratory movements Respiratory center is inhibited
PHASE 3 – FORCEFUL EXPULSION
Stomach does not actively expel
Stomach, esophagus, and & sphincters relaxed during vomiting
Force that expels arises from the contraction of the diaphragm & abdominal muscles
What is the pathway for vomiting?
PHYSIOLOGY OF VOMITING
Activation of chemoreceptors & mechanoreceptors
Stimulation of visceral afferent receptors (5-HT3; NK-1)
Direct stimulation of the cerebral cortex & limbic system – fear, stress, trauma Vestibular system stimulation (M1-cholinergic; H1-histaminergic)
CRTZ (Chemoreceptor Trigger Zone)
Simulated by vestibular system
Many receptors
Free nerve endings bathed in CSF - lacks BBBstimulated by ‘emetogens’
Kinetosis’
Motion sickness = ‘Kinetosis’
Inner ear/labyrinth stimulationdopamine and serotonin released from CRTZ activationAch released from emetic center
Drugs such as chemo-agents
5-HT3 Serotonergic Receptors & CRTZ
ACUTE VOMITING & ‘NOT ILL’
Medical Management
Antacid +/- fluid therapy and time
Anti-nausea can suppress normal vomiting response to expel FB Don’t mask with meds
Water and food
No water for 6-8 hours then small frequent amounts working back to normal over 24-48 hours
If no vomiting, small meals every 4-6 hours for day 1 with bland diet (i.e. chicken and rice or cooked beef and rice) or prescription diet
WHY SYMPTOMATIC TREATMENT ?
We don’t always have the immediate answer -support while we embark of diagnostic process
Dehydration
-can be progressive & debilitating
Patient comfort
-nausea, abdominal pain
Electrolyte imbalances
-can lead to systemic consequences if left untreated
H2 RECEPTOR ANTAGONISTS
Affects gastric parietal cell receptors
Limits acid secretion (antacid) with mild to little affect on pH
Famotidine
0.5 - 1 mg/kg PO BID
Ranitidine (also prokinetic)
1-2 mg/kg IV, PO, SQ, IM BID-TID 2.5 (IV) -3.5 (PO) mg/kg BID
Cimetidine – more Rx interactions than above 2
PROTON PUMP INHIBITOR
Gastric proton pump inhibitor antacid
Inhibits transport of hydrogen ions into the stomach
Inhibits the hepatic cytochrome P-450 mixed function oxidase system
Must check for drug interactions
Pantoprazole – IV 0.7-1 mg/kg IV SID
Omeprazole - PO 0.5-1 mg/kg SID-BID
ANTIEMETIC MEDICATIONS
Block/compete with neurotransmission at the receptor sites associated with emesis
Many off-label – veterinary studies are VERY limited Examples:
Anticholinergics Antihistamines Dopamine antagonists Serotonin antagonists Phenothiazines
NK-1 receptor inhibitors
M1-CHOLINERGIC RECEPTOR ANTAGONISTS
Scopalamine – crosses BBB, causes excitement in cats Phenothiazines (Chlorpromazome, Prochlorpromazone) Propantheline & isopropamide – peripheral/PNS action
Not Used Often Sedation Hypotension
HISTAMINE ANTAGONISTS
Not helpful for cats – no histamine receptors on CRTZ
EXAMPLES: Diphenhydramine
2.2 mg/kg PO BID-TID or IM Meclizine
4 mg/kg PO once daily
12.5 mg – 50 mg per dog PO SID 6.25-12.5 mg PO per cat PO SID
Cyproheptadine (used more for appetite stimulation)
D2-DOPAMINERGIC ANTAGONIST
METOCLOPRAMIDE
Stimulus on movement of distal esophagus cats >> dogs Antiemetic dog >> cat (fewer CNS dopamine receptors) Multiple drug interactions
5-HT3 antagonist & 5-HT4 agonist
SEs: constipation, mentation change
DOSE: IV CRI 1-2mg/kg per DAY (over 24 hours)
PO 0.2-0.5 mg/kg PO, SQ, IM BID-QID