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dyspepsia
also known as indigestion; discomfort while digesting
nausea
the inclination to vomit or as a feeling in the throat or epigastric region alerting an individual that vomiting is imminent
retching
the labored movement of abdominal and thoracic muscles before vomiting
vomiting
referred to medically as emesis
emesis
the ejection or expulsion of gastric contents through the mouth and is often a forceful event
hematemesis
vomiting of blood
1 in 4
How many individuals in the US experience repeated or chronic dyspepsia (NIDDK)?
organic dyspepsia and functional dyspepsia
What are the 2 subcategories of repeated dyspepsia?
organic dyspepsia
where dyspepsia is a sign of an underlying pathology-gastritis, gastric reflux, H pylori infection
functional dyspepsia
where dyspepsia is not accompanied by any clinical signs of damage
20%
What % of ppl seek medical care for repeated dyspepsia?
75%
What % of ppl with chronic dyspepsia show no signs of underlying damage?
symptom
Dyspepsia is a ___________-based state.
clinical presentation of dyspepsia
-discomfort
-epigastric pain or burning
-early satiety
-postprandial fullness distress
functional dyspepsia
-repeated dyspepsia with no overt signs of damage detected with imaging (endoscopy)
-underlying cause unclear
-difficult to treat without a known cause, may require ruling out therapies
•Alterations in rate of gastric emptying- rapid, delayed or dysrhythmic
•Visceral hypersensitivity
•Inflammatory cells (eosinophils, mast cells, lymphocytes) downstream in the duodenum causing irritation upstream
•Mucosal failure
•Early signs of gastritis, gastroesophageal reflux, infection
•Psychological
What are some of the underlying causes of functional dyspepsia?
Proton pump inhibitors, motility regulators, neuropsychiatric medications
What are some examples of ruling out therapies for functional dyspepsia?
EVERYONE
Who experiences nausea and vomiting?
nausea and vomiting
•May occur transiently with no other signs or symptoms
•May be part of a more complex clinical presentation
simple nausea and vomiting
-Self-limiting, resolves spontaneously, and requires only symptomatic therapy
-patient complaint of queasiness or discomfort
complex nausea and vomiting
-Not relieved after administration of antiemetics; progressive deterioration of patient secondary to fluid-electrolyte imbalances; usually associated with noxious agents or psychogenic events
-weight loss; fever; abdominal pain
serum electrolyte concentrations; upper/lower GI evaluation
What are the laboratory tests for complex?
-abdominal muscles
-stomach
-esophageal sphincter
-esophagus
-saliva production
-breathing rate (epiglottis closure)
What parts of your body coordinate activity to vomit?
pylorus and antrum contract, gastric cardia expands
What happens in the stomach during vomiting?
bidirectional
The brain-gut axis is a _____________ communication network.
Nuclei
_________ within the brainstem serve as the connection point for rapid coordination of the vomit reflex.
Cranial nerves VII (facial), IX (hypoglossal)
many roles include sensory innervation of pharynx and epiglottis as well as autonomic control of much of GI tract (critical for gag reflux)
splanchnic nerves
sense noxious stimuli in GI
enteric nervous system
is embedded in the wall of the GI tract (sensory and motor control across GI)
cortex, thalamus, hypothalamus, vestibular system
What parts of the upper CNS brain regions provide input from the brain stem in vomiting?
vomiting center (VC)
-solitary tract nuclei, dorsal motor nucleus of the vagus
-integrates signals and initiates efferent signaling (ACh) to the salivation center, respiratory center, and the pharyngeal, GI, and abdominal muscles= vomiting
VII, IX, X and visceral afferents from enteric nervous system
The vomiting center receives input from where?
chemical and mechanical triggers
bad taste, bacterial infection, over-ate, GI blockage
M1, 5-HT3, NK-1 and H1
What are the key neurotransmitter receptors in the vomiting center?
chemoreceptor trigger zone
-associated with chemically induced vomiting
-located in the area postrema of the fourth ventricle of the brain which makes it uniquely positioned to detect blood-borne and cerebrospinal fluid toxins and/or signals of GI distress
5-HT3, D2, and M1
What are the points of drug intervention in the chemoreceptor trigger zone?
informational
Increased blood alcohol and acetaldehyde activates (directly and indirectly) leads to 5-HT3 and D2 activation in CTZ
informational
Some opioids, like fentanyl, activate CTZ via D2 and the mu opioid receptors
informational
Human chorionic gonadotropin activates CTZ via M1 signaling
informational
Chemotherapies increase GI production of serotonin which triggers CTZ 5-HT3 receptor activation
motion sickness
-vestibular system within labyrinth of inner ear signals to vestibular nuclei in brain stem
-ACh to M1
-Histamine to H1
-vestibular nuclei then send signal to CTZ (5-HT3)
-CTZ to VC to vomit response
VC (vomiting center)
The cortex and thalamus send signals directly to _______ to induce vomiting.
Acute CINV
•Free radicals generated by the chemotherapeutic agent stimulates 5-HT release from enterochromaffin cells
•5-HT activates 5-HT3 receptor
•Vomiting reflex initiated
delayed CINV
•5-HT3 plays less of a role
•The chemotherapeutic agent initiates signaling pathways that lead to the release of substance P from neurons in the CNS and PNS
•Substance P activates NK1 receptors
•Vomit reflex initiated
Anticipatory CINV
the upper CNS regions are likely involved, as it is generally regarded as a conditioned response to the oncoming insult
when a patient experiences nausea when entering the chemotherapy room
What is an example of anticipatory CINV?
acute type of CINV
nausea and/or vomiting occurring within 24 hours of chemo admin
delayed type of CINV
nausea and/or vomiting occurring at least 24 hours post chemo admin; often peaks between 48 and 72 hours
breakthrough type of CINV
nausea and/or vomiting that occurs within 5 days post chemo despite optimal antiemetic regimen used; requires rescue therapy with other antiemetics
refractory type of CINV
nausea and/or vomiting that occurs in subsequent chemo cycles despite maximum antiemetic protocol
anticipatory type of CINV
nausea and/or vomiting that is triggered by sensory stimuli associated with chemo admin
cyclic vomiting syndrome
-characterized by sudden repeated episodes of nausea and vomiting lasting from a few hours to several days
-etiology is unkown
cannabinoid hyperemesis syndrome
-condition in which a patient experiences cyclical nausea and vomiting and abdominal pain after using cannabis
-etiology: cannabis use; mechanism poorly understood but involves TRPV1 (does resolve after cannabis use ends)
petichiae
from intravascular pressure spikes when straining
-aspiration
-dehydration
-malnutrition
-pharyngitis
-esophagitis
-tooth decay
What are some complications of nausea and vomiting?
prevent or eliminate nausea and vomiting
What is the overall treatment goal for nausea and vomiting?
non-pharmacological management of nausea and vomiting
dietary, physical, or psychological strategies
pharmacologic treatment for nausea and vomiting
-target underlying triggers, such as treating infections or altering medication regimen if medication associated
-block signaling in CTZ and or VC
5-HT3, M1, H1
What are the most antiemetics used in blocking for N/V treatment?