Unit 11 Flashcards
two distinct medullary centers for vomiting
vomiting and chemoreceptor trigger zone
emesis
vomiting
hypoxia exerts direct effect on
vomiting center
what are some neurotransmitters that work on chemoreceptors for the vomiting
dopamine, serotonin, opioid
do we want excess or little of dopamine, serotonin, opioids
we want little
why do we want to attack dopamine, serotonin, opioid
to prevent nausea
where is the chemoreceptor trigger zone located
small area on the floor of the fourth ventricle
the chemoreceptor trigger zone is exposed to
blood and cerebrospinal fluid
the chemoreceptor trigger zone is thought to mediate the emetic effects of
blood borne drugs and toxins
swallowing depends on the coordinated action of the
tongue and pharynx
swallowing structures are innervated by cranial nerves
V (5), IX (9), X (10), XII, (12)
dysphagia
difficulty in swallowing
Odynophagia
painful swallowing
achalasia
failure of the esophageal sphincter to relax
Mallory-Weiss Syndrome
non penetrating mucosal tears at gastroesophageal junction
Gastroesophageal Reflux Disease (AKA Gerd)
heart burn
GERD can lead to cancer how?
constant inflammation and then healing cycle
GERD pain is easily confused with
angina
Barret esophagus squamous replaced by
columnar
Barret esophagus can lead to
cancer
GERD in children commonly will present with
evidence of pain when swallowing, irritability, inconsolable crying
GERD in children may cause
respiratory problems, dental carries or ear pain
how do you get dental carries with GERD in children
because acid errodes the enamle
GERD children are very
colicly
two types of gastric mucosa
water insoluble and water soluble
water insoluble mucus forms
thin, stable gel that adheres to the gastric mucosal surface
water soluble mucus is ______ and it is a lubricant that prevents mechanical damage to the mucosal surface
viscid
Gastric Mucosal barrier is
impermeable epithelial cell surface
Gastric Mucosal Barrier mechanism for selective transport of ________ and ____ ions and characteristics of gastric mucosa
hydrogen, bicarb
ASA is non ionized and lipid soluble rapidly diffuses increases
mucosal permeability and damages epithelial cells
prostaglandin role
secrete bicarb
shock affects the
protaglandin
if you are in shock you will have more acid why?
prostaglandins are not working
Acute gastritis can or cannot heal its self
can heal itself
transient
short term
Acute Gastritis is transient inflammation of
gastric mucosa
acute gastritis inflammation is caused by
bacterial endotoxins, alcohol or asprin
acute gastritis severity ranges from
edema to hemorrhagic erosin
acute gastritis is self limiting with complete regeneration and healing within
days
Chronic Gastritis is transient or not transient
not transient
what is the most common cause of chronic gastritis is
H. Pylori
what else could cause chronic gastritis
autoimmune
how to get rid of H. Pylori
antibiotics
H. Pylori colonizes the
mucus secreting epithelial cells of the stomach
H. Pylori bacteria have what that allow them to move through the mucous layer of the stomach
multiple flagella
H. Pylori secretes _______ which enables them to produce sufficient ammonia to buffer acidity of their environment
urease
H. Pylori produce _______ and ______ that interfere with mucosal protection against injury from gastric acid
enzymes, toxins
second most common cause of Chronic Gastritis
NSAIDs
H. Pylori causes damages to the stomach lining which could lead to what 2 issues
ulcers or increased risk of gastric cancer
When you take Aspirin/NSAIDs those drugs inhibit the synthesis of prostaglandins leading to
increased acid production because acid production is regulated by prostaglandins so when you inhibit them you have unregulated acid production
NSAIDs and aspirin contribute to the formation of gastritis by inhibiting the
synthesis of prostaglandins
when you take NSAIDs/asprin the synthesis of prostaglandins is decreased due to the __________ action of the drug; there for ____ _________ is unregulated
anti inflammatory, acid production
why would the c urea breath test with when testing for H. Pylori
because they released urease
ways to test for H. Pylori
C urea breath test, stool antigen test
C urea breath test using
radioactive carbon isotope
Peptic ulcer disease can be caused by
H. Pylori, use of ASA and NSAIDs
peptic ulcer you get discomfort and pain when the stomach is empty or full
empty
melena
black tarry stool
stress curling happens when you have
massive burns
cushings is increased
cranial pressire
you get cushings after
injury, operation, tumors
complications of peptic ulcers
hemorrhage, obstruction, perforation
hemorrhage does or does not go through the wall
can happen when the ulcer doesn’t go through the wall
hemorrhage
caused by bleeding from granulation tissue or from erosion of an ulcer into an artery or vein
obstruction caused by
edema, spasm, or contraction of scar tissue and interference with the free passage of gastric contents through the pylorus or adjacent areas
perforation occurs when an ulcer erodes
through all the layers