Vomiting Flashcards

1
Q

The following describes what?

A reflex
Forceful expulsion of stomach contents through the mouth
One of the most common presentations of illness in our patients
Self limiting vs. debilitating

A

Vomiting!

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2
Q

What are the 3 phases of vomiting?

A

Nausea
Retching
Expulsion

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3
Q

What clinical signs are associated with the first phase of vomiting (nausea aka prodromal phase)?

A

Ptyalism

  • Hiding*
  • Seeking attention*
  • Yawning*
  • Shivering*
  • Tachycardia*
  • Pallor*
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4
Q

What clinical signs are associated with the second phase of vomiting (retching)?

A

Abdominal mm, chest wall and diaphragm all contract without any expulsion of gastric contents

Retrograde contraction –> duodenal contents into stomach

Deep inspiratory movements

Respiratory center is inhibited

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5
Q

What clinical signs are associated with the third phase of vomiting (forceful expulsion)?

A

Stomach DOES NOT actively expel!!

**Stomach, esophagus, and sphincters relaxed during vomiting!!

Force that expels arise from the contraction of the diaphragm and abdominal mm

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6
Q

What is the pathway for vomiting?

A

Stimuli –> afferent pathways (sensory and central); higher brain; vestibular apparatus (motion sickness); CRTZ –> emetic center –> efferent motor signals = VOMIT TME!

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7
Q

Explain the physiology of vomiting.

A

Activation of chemoreceptors and mechanoreceptors
Stimulation of visceral afferent receptors (5-HT3; NK-1)
Direct stimulation of the cerebral cortex and limbic system -fear, stress, trauma
Vestibular system stimulation (M-1 cholinergic; H1-histaminergic)
CRTZ (Chemoreceptor Trigger Zone)
-stimulated by vestibular system
-many receptors
-free nerve endings bathed in CSF -lacks BBB –> stimulated by ‘emetogens’

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8
Q

How does motion sickness (“kinetosis”) induce vomiting?

A

inner ear/labyrinth stimulation –> dopamine and serotonin released from CRTZ activation –> Ach released from emetic center

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9
Q

How do drugs such as chemo agents induce vomiting?

A

5-HT3 serotonergic receptors and CRTZ

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10
Q

How does intestinal inflammation induce vomiting?

A
  • direct afferent input to vomiting center

- many causes of GI dz; pancreatitis

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11
Q

How do opioids induce vomiting?

A

-stimulation of CRTZ, increased vestibular sensitivity, gastric stasis, or impaired intestinal motility and constipation

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12
Q

How do toxins induce vomiting?

A

-CRTZ permeable and initiates NT cascade

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13
Q

How does uremia induce vomiting?

A
  • decreased gastric clearance –> ulcers and gastritis (PPI, H2-antag)
  • toxins cross BBB –> stimulate central and peripheral receptors
  • activates CRTZ via D2-dopaminergic receptors
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14
Q

T/F When a client tells you their pet never eats anything that they shouldn’t you should believe them bc they know their pets best.

A

False. People don’t know shit.

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15
Q

What clinical signs do we see with vomiting?

A
vomiting
lethargy
inappetence 
\+/- diarrhea
\+/- wt loss
systemic signs of illness 
respiration changes if aspiration has occurred
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16
Q

There are some major things to note when performing physical exam with a dog that’s vomiting. What are they?

A
  • dehydration- skin, eyes
  • abdominal pain
  • abdominal distension
  • palpable foreign material
  • thickened intestines
  • constipation (bc straining so much in litter box they make themselves vomit)
  • normal
  • ptyalism
  • mental status (toxins, CNS dz)
  • respiratory status-can change
  • diarrhea (do a rectal!)
  • **look under the tongue!!
  • wt loss
  • signs of systemic illness
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17
Q

Diagnostics are sorta the same as always but what’s something additional that’s unique with regards to vomiting?

A

Baseline cortisol is an extra aspect of diagnostic workup to look into as well as coagulation profile (i.e. if hematemesis or protein losing nephropathy)

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18
Q

T/F DO NOT make initial recommendations based on owner finances.

A

True

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19
Q

What is your protocol when patient is NOT systemically ill and is acutely vomiting?

A

Symptomatic therapy; few days of diet and medications then wean onto normal diet

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20
Q

What is your protocol when patient IS systemically ill and is acutely vomiting?

A

Symptomatic therapy; lab evaluation and imaging

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21
Q

What is your protocol when patient is NOT systemically ill and is chronically vomiting?

A

Symptomatic therapy; food trial at least 2 -3 wks; +/- Medication trials

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22
Q

What is your protocol when patient IS systemically ill and is chronically vomiting?

A

Symptomatic therapy; lab evaluation and imaging; +/- biopsy

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23
Q

What are the basics to know about PCV/TS?

A
PCV= estimate of RBC
decreased= anemia 
increased= dehydration 
TS= total solids= serum proteins- mostly Alb and globulins, as well as fibrinogen and other proteins
decreased= low protein
increased= dehydration, some advanced inflammatory dz and neoplasia
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24
Q

What are some basics to know about Blood glucose?

A
BG= blood glucose 
decreased= hypoglycemia from various cause 
increased= possibly DM

On many glucometers –> affected red cell count
decreased= artificially w polycythemia
increased= dehydration

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25
Q

Serum chemistry rules out what ?

A

kidney, liver and electrolyte concerns

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26
Q

Urinalysis helps rule out what?

A

UTI and UTO; indicators of other systemic dz

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27
Q

Fecal tests help rule out what?

A

Parasites

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28
Q

Coags help rule out what?

A

if hematemesis or other signs of bleeding are present

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29
Q

When would we perform a baseline cortisol?

A

to rule out Addison’s or support pursuing ACTH stim

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30
Q

When would we perform a PLI?

A

To check for pancreatitis

31
Q

T/F It is fine to just take abdominal ultrasound and not perform x rays.

A

False! US does not take the place of X rays!

32
Q

How do we treat patients with acute vomiting but “not ill”?

A

medical management: antacid +/- fluid therapy and time . . . anti nausea can suppress normal vomiting response to expel FB - SO DONT MASK WITH MEDS! Let dem vomit

33
Q

T/F In patients that are acute vomiting but “not ill,” water should be withheld for 6-8 hours with small, frequent amounts working back to normal over 24-48 hours. If not vomiting, small meals should be given every 4-6 hours for day 1 with bland diet or prescription diet.

A

True. Bland diet= chicken and rice or beef and rice or prescription diet

34
Q

How do we administer outpatient fluids?

A

SQ or IV bolus

35
Q

When giving an outpatient treatment fluids, the volume will depend on the hydration status. Typically, the hydration status is mild which means we give what fraction of their daily maintenance?

A

1/3- 1/2 daily maintenance

36
Q

If a 10 kg dog is being given outpatient fluids, how many mLs would he be given if his maintenance is 60 mLs/kg/day?

A

200-300 mLs because 10 x 60= 600 and then we give 1/3-1/2 of daily maintenance

37
Q

What is the shock dose needed for rehydration?

A

60-90 mLs/kg; start w 1/4-1/3 then reassess

38
Q

What are the risks of fluid therapy?

A

History of heart failure (volume overload so consider enteral water via nasogastric tube) and severe hypoproteinemia (can easily induce edema, effusions)

39
Q

Normosol, Plasmalyte, LRS and Sodium Chloride 0.9% are all considered maintenance fluids. How are they administered?

A

SQ/IV

40
Q

Explain the MOS of H2 Receptor Antagonists.

A

Affects gastric parietal cell receptors. Limits acid secretion (antacid) with mild to little affect on pH.

41
Q

Famotidine, Ranitidine and Cimetidine are al examples of wut?

A

H2 Receptor Antagonists

Cimetidine has more Rx interactions than the other 2

42
Q

Explain the MOS of PPIs (Proton Pump Inhibitors).

A
  • gastric proton pump inhibitor antacid
  • inhibits transport of hydrogen ions into the stomach
  • inhibits the hepatic cytochrome P-450 mixed fxn oxidase system
  • MUST check for drug interactions
43
Q

Pantoprazole and Omeprazole are examples of what?

A

PPIs

44
Q

Explain the MOS of Antiemetic medications.

A

Block/compete with neurotransmission at the RECEPTOR SITES associated with emesis

45
Q

Anticholinergics, antihistamines, dopamine antagonists, serotonin antagonists, phenothiazines and NK-1 receptor inhibitors are all examples of what?

A

Antiemetic medications

46
Q

M1- Cholinergic Receptor Antagonists (Scopalamine, Phenothiazines, Propantheline and isopropamide) are not used very often. Why?

A

They cause sedation and hypotension

47
Q

T/F Histamine antagonists can be safely used on cats.

A

False. Not helpful for cats bc no histamine receptors on CRTZ.

48
Q

Diphenhydramine, Meclizine and Cyproheptadine are all examples of what?

A

Histamine antagonists.

49
Q

Metoclopramide is an example of what?

A

D2-dopaminergic antagonist . . . know this mother fucker!

50
Q

Explain the MOS of Metoclopramide.

A

Stimulus on movement of distal esophagus. Cats» dogs.

Antiemetic: Dogs&raquo_space; cats (few CNS dopamine receptors)

Multiple drug interactions

5-HT3 antagonist & 5-HT4 agonist

51
Q

What are the SE’s of Metoclopramide?

A

Constipation, mentation change

52
Q

Where do 5-HT3- Serotoin antagonist work?

A

Work in GI tract & CRTZ

53
Q

What are the SEs oF 5-HT3- Serotoin antagonist?

A

constipation (she sees this a lot), fatigue, dry mouth

54
Q

Anzemet and Zofran are examples of what?

A

5-HT-Serotoin Antagonists

55
Q

How do NK-1 Receptor Antagonists work?

A

Competes with Substance P peripherally and centrally

56
Q

Cerenia is an example of what?

A

NK-1 Receptor Antagonists. . . she looooves her some Cerenia

57
Q

What are the SE’s of Cerenia?

A

ataxia, anorexia, diarrhea, injection soreness, bradycardia w high dose

58
Q

Cerenia is used to tx vomiting and what else?

A

Motion sickness! Need higher dose when tx motion sickness.

59
Q

Carafate is a what?

A

Gastric mucosal protectant

60
Q

How does Carafate work?

A

Stimulates PG E2 & I1- cytoprotective
Reacts w HCl to form paste which sticks to ulcers
Inactivates pepsin and binds bile acids
Binds GI phosphorous
Weak antacid

61
Q

When should Carafate be given?

A

2 hours before or after other meds and food

62
Q

Metoclopramide, Cisapride, Ranitidine and Erythromycin are all what?

A

Prokinetics!

63
Q

How do 5-HT4 Receptor Activators work?

A

Gastric emptying and GI motility
Stimulate release of Ach into the enteric NS
LES, stomach, colon

64
Q

Cisapride and Metoclopramide are examples of what?

A

5-HT4 Receptor Activators

65
Q

Cisapride works really well for constipation tx in what species?

A

Cats!

Cisapride, Constipation, Cats.

C’s get degrees.

66
Q

How do macrolide antibiotics work?

A

Stimulates Motilin
Promotes intestinal motility
Initiates phase III of migrating myoelectric complex which propels ingesta

67
Q

What’s an example of a macrolide antibiotic?

A

Erythromycin

68
Q

T/F Withholding food is appropriate with chronic vomiting.

A

False. Withholding food is NOT appropriate with chronic vomiting.

69
Q

T/F You should not perform a food trial if animal is systemically ill.

A

True. Why try and fuck with them when they’re sick? Leave them alone. Deal with food changes later.

70
Q

Cyproheptadine is an H1 receptor blocker and serotonin antagonist. Why do we utilize it in vomiting?

A

It’s a appetite stimulant!

71
Q

How does Tetracyclic antidepressants work as appetite stimulants?

A

They increase NE and thus appetite

72
Q

Mirtazapine is an example of what?

A

Tetracyclic antidepressant

73
Q

What are some SE’s of Mirtazapine?

A

Polyphagia, sedation or excitement

74
Q

Clicker Q: Cerenia works by which mechanism?

A. Serotonin receptor (5-HT3) antagonist
B. Substance P competitor at NK-1 receptor
C. Magic
D. PPI

A

B! Substance P competitor at NK-1 receptor