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Clin med A 2 > L1 - Nausea and Vomiting > Flashcards

L1 - Nausea and Vomiting Flashcards

1
Q

what are the major physiologic functions of the GI system (just the basic functions)

A
  1. digest food
  2. absorb nutrients into blood stream
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2
Q

what happens to unabsorbed nutrients and wastes in the GI system

A

they are collected in te large intestine for elimination

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3
Q

What are the functions of the GI system

A
  1. ingestion - solid food and liquid enter oral cavity
  2. mechanical digestion and propulsion - crushing/shredding of food in oral cavity and churning in stomach
  3. chemical digestion - chem and ezymatic breakdown of food into small organic molecules that can be absorbed by the digestive epithelium
  4. secretion - The release of water, acids, enzymes, buffers, and salts by the digestive tract epithelium and by accessory organs
  5. absorption - Movement of nutrients across the digestive epithelium and into the bloodstream
  6. defecation - indigestible foods are compacted into material waste that is eliminated by defecation
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4
Q

what three parts is the GI system broken into? what do each contain?

A
  1. upper - mouth, esophagus, stomach
  2. middle duodenum, jejunum, ileum
  3. lower - cecum, colon, rectum
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5
Q

What features of the GI system increase surface are for absorbing nutirents

A

its lined with permanent ridges and temporary folds (stomach rugae)

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6
Q

what are the accessory organs of the GI system? what are their jobs?

A
  1. salivary glands
  2. liver
  3. pancreas

these produce secretions to aid in digestion

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7
Q

what is the definition of vomiting

A
  • Usually follows nausea, including retching (spasmodic respiratory and abdominal movements)
  • Oral expulsion of gastrointestinal contents due to contractions of the gut and thoracoabdominal wall musculature
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8
Q

what is regurgitation

A
  • The effortless reflux of liquid or food stomach contents
  • “Burping up” food contents
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9
Q

what is rumination

A

The chewing and swallowing of food that is regurgitated after meals

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10
Q

the motor function of the gut is controlled at three main levels…. what are they?

A
  1. parasympathetic and sympathetic nervous system
  2. enteric brain neurons
  3. smooth muscle cells
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11
Q

normal function of the GI tract involves what interaction?

A

interaction between the gut and the CNS

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12
Q

what does nausea correlate with

A

with a shift in the normal 3-cycle-per minute gastric myoelectrical activity (muscle contraction and relaxation)

stomach should contract and relax every 3 min. nausea disrupts this

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13
Q

what is tachygastria

A

increased rate of electrical activity in the stomach (4+ cycles/min)

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14
Q

what is bradygastria

A

decreased rate of electrical activity in the stomach (less than 2 cycles)

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15
Q

what are the 4 different sources that can stimulate vomiting

A
  1. afferent vagal fibers from the GI viscera - rich in serotonin 5-HT3.
  2. fibers of the vestibular system - high concentrations of.histamine H1.
  3. higher CNS centers
  4. chemoreceptor trigger zone - rich in opioid, serotonin 5-HT3, neurokinin 1, and dopamine 2 receptors.
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15
Q

what could cause vomiting via stimulation of the afferent vagal fibers from GI viscera

A

GI distention, mucosal or peritoneal irritation, infections

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16
Q

what could cause vomiting via stimulation of the Fibers of the vestibular system

A

sea- sickness
dizziness

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17
Q

what could cause vomiting via stimulation of Higher CNS centers

A

certain sights, smells, or emotional experiences may induce vomiting

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18
Q

what could cause vomiting via stimulation of chemoreceptor trigger zones

A
  • this is located outside blood-brain barrier in the area postrema
  • stimulated by drugs, chemo agents, toxins, hypoxia, uremia, acidosis, radiation therapy
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19
Q

what steps should be followed in both urgent care and outpatient setting for patients with nausea/vomiting

A
  1. seek out etiology and take into account whether s/s are acute or chronic
  2. identify consequences or complications of n/v (fluid depletion, hypokalemia, met alkalosis)
  3. provide target therapy when possible (surgery for bowel obstruction or malignancy)
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20
Q

what are some typical causes of acute symptoms w/o severe abd pain

A

should be asked about med, diet changes and sick contacts
also
* typically caused by food poisoning
* infectious gastroenteritis
* drugs
* systemic illnesses

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21
Q

what is suggested by acute onset of severe abdominal pain and vomiting

A
  • suggests peritoneal inflammation
  • acute gastric/intestinal obstruction
  • pancreatobiliary disease
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22
Q

what could persistent vomiting suggest?

A
  • suggests pregnancy
  • gastric outlet obstruction
  • gastroparesis
  • intestinal dysmotility
  • psychogenic disorders (think bulimia)
  • CNS/systemic disorders
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23
Q

what does morning vomiting suggest?

A
  • pregnancy
  • uremia
  • alcohol intake
  • increased intracranial pressure
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24
Q

what should you suspect in patients with a hx of cannabis use

A

cannabinoid hyperemesis syndrome

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25
Q

how does cannabinoid hyperemesis syndrome present

A
  • recurrent episodes of NV and ab discomfort
  • typically occurs in younger adults with hx of frequent chronic cannabis use
  • improvement with hot shower or bath
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26
Q

what should you suspect if a patient vomits immediately after meals

A
  • bulimia - TEETH EXAM
  • other psychogenic causes
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27
Q

what should you suspect if a patient vomits undigested food one to several hours after meals

A
  • gastroparesis
  • gastric outlet obstruction - may hear a succussion splash
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28
Q

what neurologic symptoms should you ask about with NV

A

headache
stiff neck
vertigo
focal weakness/paresthesias
feculent vomiting = intestinal obstruction

29
Q

what is hematoemesis

A

vomiting of blood or coffee like material

30
Q

what lab studies should be ordered for CC of NV, why?

A
  • CBC - infection, anemia
  • CMP - Electrolyte disturbances, liver function, azotemia, metabolic alkalosis from loss of gastric contents
  • Amylase and lipase - pancreatic enzymes
  • b-hCG
31
Q

what imaging could you do in a patient whose CC is NV

A

Xrays - flat and upright abdominal films

usually only in pts with severe or suspicion of mechanical obstruction

32
Q

what would Xrays show in small bowel obstruction

A

intestinal air-luid levels with reduced colonic air

33
Q

what would Xrays show in ileus

A

diffusely dilated air-filled bowel loops

34
Q

what additional testing may be done in NV if initial testing is non-diagnostic

A
  • EGD - ulcers, malignancy, obstruction, food residue.
  • CT scan - partial SBO
  • colonoscopy - detects colonic obstruction, malignancy, inflammatory conditions
  • US - intraperitoneal inflamm, choleslithiasis
  • MRI - inflammation in chrons
  • GI motility testing - underlying motor disorders, delayed gastric emptying, functional dyspepsia
35
Q

what are complications of NV

A
  • Volume Depletion/Dehydration
  • Electrolyte Disturbances
  • Aspiration
  • Mallory-Weiss Tear
  • Boerhaave Syndrome (Esophageal Rupture)
36
Q

what is the treatment for NV

A
  • correct abnormalities if possible
  • hospitalization if dehydration
  • once oral intake is tolerated and restarted on low fat liquids
37
Q

why do we use low fat liquids when reintoducing food to patients recovering from NV

A

because lipids delay gastric emptying

38
Q

what is the tx for mild-moderate NV

A
  • Clear liquids (broths, tea, soup, carbonated beverages)
  • Advance to small quantities bland food (crackers)
  • Antiemetic medication
39
Q

what is the treatment for mod-severe NV

A
  • Hospitalization with IV (isotonic) fluids
  • Antiemetic medication
  • NG tube in certain situations (i.e. small bowel obstruction/gastric)
40
Q

children and infants with difficult IV/IO access can be rehydrated using what?

A

NG tube:(

41
Q

how is oral rehydration achieved in a pediatric patient

A

by giving 50–100 mL/kg of a glucose–electrolyte solution over 4 hours. In children, age-appropriate diet and breast-feeding may resume as soon as possible. In either case, start with small doses of oral fluid and slowly increase the amount.

42
Q

what is the goal of fluid replacement therapy

A

The goal of replacement therapy is to correct existing abnormalities in volume status and/or serum electrolytes.

43
Q

how do you assess volume deficit

A
  • weight loss ( if pre and post fluid loss weight is known)
  • clinical and lab parameters (BP, jugular venous pressure, urine Na conc, urine output.)
44
Q

what is the rate of replacement for severe volume depletion or hypovolemic shock

A
  • at least 1 or 2 liters of isotonic fluids given as rapidly as possible in an attempt to restore tissue perfusion
  • contones at a rapid rate until clinical signs of hypovolemia improve
45
Q

what is the rate of replacement for mild-mod hypovolemia

A
  • rapid fluid resuscitation is not necessary
  • Induce positive fluid balance = administration of fluid at a rate that is 50 to 100 mL/hour greater than estimated fluid losses.
46
Q

what types of fluid replacement would be needed in certain electrolyte disorders

A
  • regular hypovolemia = isotonic saline
  • hyper/hyponatremia should be corrected slowly since rapid correction is harmful
  • potassium depletion = potassium replacement
  • metabolic acidosis = sodium bicarb
47
Q

Caution with parenteral fluid bolus doses in following patient populations:

A

infants, patients with poor systolic ejection fraction, kidney disease, chronic severe hyponatremia (without neuro deficits that require hypertonic saline) and DKA in children.

48
Q

what class drug is ondansetron (zofran) and what is the MOA

A
  • class is serotonin 5-HT3 receptor antagonist
  • MOA = 5-HT3 receptors present both peripherally and centrally, Blocks serotonin from binding to 5-HT3 receptors, Blocking stimulation of “vomiting center” in medulla
49
Q

what are indications for ondansetron (zofran)

A
  • Acute N/V
  • Postoperative N/V
  • Chemotherapy related N/V
  • Hyperemesis gravidarum? (avoid in 1st trimester d/t rare chance of cleft palate)
50
Q

how is ondansetron (zofran) metabolized

A

by the liver

caution in hepatic impairment

51
Q

what should you monitor for in the use of ondansetron (zofran)

A
  • if patient is pregnant
  • QT prolongation
52
Q

what are SE of ondansetron (zofran)

A
  • HA
  • Diarrhea/Constipation
  • Fatigue, malaise
  • Dizziness
  • Pruritus
53
Q

what class is Scopolamine (transdermscop)/ meclizine/doxylamine and what is the indications for this drug

A
  • anticholinergic/antihistamine
  • indicated in Motion Sickness, vertigo, migraines. COmbined with oral Vitamin B6 and doxylamine for pregnancy (1st line in NV while pregnant).
  • also indicated in post operative NV
54
Q

what are common SE of scopolamine/meclizine/doxylamine? what is the dosage form of this med

A
  • xerostomia, urinary retention
  • dizziness
  • drowsiness, mydriasis
  • dosage form = patch!
55
Q

what class is promethazine (phenergan). what is it indicated for

A
  • class - 1st generation antihistamine; blocks H¹ receptors, special mention for Dopamine Receptor Antagonist (Phenothiazine); with H1 blocking as well
  • indicated for acute NV
56
Q

what is promethazine (phenergan) metabolized by

A

the liver CYP450

57
Q

what are serious adverse reactions for promethazine (phenergan)

A
  • Respiratory Depression
  • Seizures
  • Leukopenia
  • Thrombocytopenia
  • Hallucinations
  • Extrapyramidal Side Effects
  • Bradycardia
58
Q

what are common SE of promethazine (phenergan)

A
  • Sedation
  • Blurred Vision
  • Confusion
  • Xerostomia
  • Dermatitis
  • Urinary retention
  • Constipation
59
Q

what is the BBW for promethazine (phenergan)

A
  • resp depression
  • tissue injury/necrosis
60
Q

what are CI for promethazine (phenergan)

A
  • resp depression
  • children under 2
61
Q

who should you caution promethazine (phenergan) in?

A
  • Elderly
  • CNS depression
  • Asthma/COPD
  • Glaucoma
  • BPH
  • Cardiac Ds
  • Hepatic Ds
  • Seizure Ds
62
Q

what pregnancy category is promethazine (phenergan)

A

category C

63
Q

metoclopramide (reglan) is what class and what is the MOA

A
  • class = prokinetic
  • Increases peristalsis primarily by inhibiting dopamine
  • enhances response to acetylcholine of tissue in upper GI
  • enhances motility and accelerated gastric emptying
  • increases lower esophageal sphincter tone
64
Q

what are indications for metoclopramide (reglan) and how is it metabolized

A
  • indications: NV, gastroparesis, refractory GERD
  • minimal liver metabolism, renally excreted
65
Q

what are serious SE for metoclopramide (reglan)

A
  • Extrapyramidal Side Effects
  • Neuroleptic malignant syndrome
  • Seizures
  • Depression/Suicidal Ideations
  • Leukopenia/Agranulocytosis
  • CHF, arrhythmias
  • HTN
66
Q

what are common SE of metoclopramide (Reglan)

A
  • Diarrhea
  • Drowsiness
  • Restlessness
  • Anxiety/Insomnia/Depression
  • HA/Dizziness
  • Hormonal Disorders
  • HTN
67
Q

what is the BBW of metoclopramide (Reglan)

A
  • tardive dyskinesia
68
Q

what are CI for metoclopramide

A
  • seizure Ds
  • GI obstruction
69
Q

what pregnancy category is Metoclopramide (reglan)

A

pregnancy category B

70
Q

what are cautions for metoclopramide (reglan)

A
  • HTN
  • Parkinsons
  • CHF
  • Depression
  • DM
  • Renal Impairment
71
Q

what are other medications that can be used for NV

A
  • neurokinin receptor antagonists (aprepitant/emend) - given during chemo with dexamethasone
  • dexamethasone - post op NV, chemo (additive agent)
  • lorazepam = benzo (xanax) anticipatory NV with chemo (given along with zofran to help with chemo induced vomiting)

Clin med A 2 (30 decks)

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