Unit 2 Flashcards
hernia
organ protrusion thru retaining str wall
where is there inc prevelance of hernias
abdm cavity
2 requirments needed for herniation to occur (patho)
weakening of supporting or retaining str
inc intra abdm pressure
what etiologies relate to weakening of supporting strs in herniations
acquired (injury, aging)
congenital (baby born w m. weakness)
what etiologies relate to inc abdm pressure
acquired (pregnancy, obesity)
hiatus
aperture opening in diaphragm for esophagus
what is a hiatal hernia
hiatus enlarges dt age(?) and inc P admn -> part of stomach enters TC
2 types of hiatal hernia
sliding
rolling
percent incidence in sliding hernia
95%
percent incidence in rolling hernia
5%
what happens in a sliding hiatal hernia
upper stomach and GEJ slide up into TC. stomach is pinched at entry point into TC
what percent of pts w sliding hiatal hernias are symptomatic
50%
what symptoms are present in pts w sliding hiatal hernias
chest pain, heart burn, reflux
what happens in a rolling/paraesophageal hiatal hernia
non upper part of stomach moves above diaphragm while GEJ remains in normal spot
mnfts of rolling hiatal hernia
chest pain
dyspnea
feeling full sooner after meals
why is there chest pain in a rolling hiatal hernia
rt anatomical repositioning of stomachq
why is there dyspnea in a rolling hiatal hernia
stomach takes up part of TC -> dec lung capacity for 02
why does the pt feel full sooner if they have a rolling hiatal hernia
dec stomach capacity AND smaller herniated pocket still fx’s normally, this mini stomach has stretch receptors so when small pocket fills -> n. sends signal of feeling full
tx for hiatal hernias
lifestyle mods
drugs for gastric reflux
sx
what lifestyle mods occur when txing hiatal hernias
avoid bending over after eating, avoid heavy meals, sleeping after meals, inc HOB to address reflux -> dec heartburn and pain
what drugs are used to treat gastric reflux in hiatal hernias
antacids
H2RA
PPI
what sx is used to treat hiatal hernias
fundoplication, reduce hernia while wrapping fundus of stomach around junction to prevent it from moving up while tightening cardiac sphincter
inguinal hernia
abdm organs protrude via inguinal ring forming hernial sac
what aperture do inguinal hernias exit from
inguinal ring
what is the inguinal ring
taught opening allowing passage of spermatic cord to exterior body
what is in a hernial sac
peritonium with organ and omentum inside
2 types of hernia
direct
indirect
direct hernia
herniation via no aperture (hiatal)
indirect hernia
herniation via present aperture (inguinal)
peptic ulcer disease
ulcerative disorder of upper GI tract (20% stomach, 80% duodenum).
why is there higher incidence of peptic ulcer disease in the duodenum
no protective lining here
what layers does peptic ulcer disease primarily affect
mucosa, deeper layers if no tx
how does peptic ulcer disease progress
with remissions and exacerbations, (acute condition that may become chronic)
ET of of peptic ulcer disease
dt inf caused by heliobacter pylori
how does heliobacter pylori colonize in the stomach
creates a niche and colonizes within stomach wall
how does heliobacter pylori attatch to stomach wall
adhesion proteins allowing attatchment to epithelial tissue
how does h pylori survive in acidic environment of the stomach
secrete Urease
what is urease
enzyme that breaks down urea
what does urease break down urea into
NH3 + CO2 -> carbonic acid buffer -> bicarbonate
how does the break down of urea aid in the survival of H pylori
urea breaks into bicarbonate which buffers pH on a small scale allowing H pylori to live
what does h pylori induce
inflm of tissue
hypergastrinemia
hypergastrinemia
inc sec of gastrin hormone
fx of gastrin
inc Hcl prod in host stomach.
risk factors/offensive factors of peptic ulcer disease
Hcl + biliary acid steroids & NSAIDS chronic gastritis smoking, alcohol, caffeine stress
which offensive factor is etiologic
Hcl and biliary acid
what is an offensive factor
things that increase aggrevation of peptic ulcer disease
which offensive factor is different then the rest? why
chronic gastritis
its presence makes a pt more susceptible to ulcers
what are defensive factors
factors that prevent ulcer formation
what 4 defensive factors prevent ulcer formation
acid regulation
intact perfusion
mucous presence
ability of mucosa to regenerate new cells
what is to be said about the relationship between offensive and defensive factors
normally, defensive factors > then offensive factors
what happens if offensive factors > defensive factors
makes pt more susceptible to ulcers if H pylori is present
patho of peptic ulcer disease (2)
H pylori infec-> inflm mediator rls -> tissue damage
infc -> inc gastrin prod -> inc acid sec -> tissue damage dt no acid regulation
mnfts of peptic ulcer disease
abdm pain
N/V
Fever
describe mnft of abdm pain in peptic ulcer disease
burning and cramping dt inflm of tissue and tissue erosion by HCLl. its felt in the chest and may be described as angina pain
why does N/V occur in peptic ulcer diesae
GI mnft
when does fever occur in peptic ulcer disease
when H pylori is first establishing
3 complications of peptic ulcer diseae
perforation of ulcer
hemorrhage
gastric obstr
what may perforation of a peptic ulcer ->
peritonitis
how does hemmorrhage of a peptic ulcer mnft?
occult blood in stools
what may a gastric obstr in peptic ulcer disease be caused by
edema
scar tissue contraction
m. spasm
mechanism of scar tissue contraction and gastric obstr
mucosa attempts to come together at points of injury pulling on the tissue around it, making area tight
which tests are use to dx PUD
Hx serology fecal Ag UBT barium swallow endoscopy
fx of serology in PUD
looking for Ab’s against H pylori in blood
fx of Fecal Ag in blood
testing stool for Ag’s related to H pylori / inc protein content
what is the number one dx in PUD
UBT
fx of UBT
pt ingests soln thats made to mark C14 if present. pt then gives breath sample 2-2.5 h later and if C14 is present h pylori is presnt
how does UBT pick up H pylori infc
H pylori breaks down urea using urease, which is normally not present. If urea is being broken down into Co2 and NH3, then the C in CO2 is available to be marked by the test. the marked CO2 is then exhaled
fx of barium swallow in PUD
we can do this to visualize extent of ulcerations
fx of endoscopy in PUD
may be used instead of ba swallow or with it, we can image ulcers this way
Tx for PUD
antacids?
triple regimen
Sx
fx of antacids in PUD
for symptom relief and OTC med thats not to be used long term dt inc risk for kidney stones
triple regimen
3 drugs used congruiently
which drug categories are used in the triple regimen
either H2RA and 2 Abx, or PPI and 2 ABx
how does an H2Ra work
block receptor for histamine binding. Normally histamine binding -> facilitates acid sec
common H2Ra’s
zantac
tagamet
how does a PPI work
blocks release of H+ from protein pumps -> dec of HCl prod
what are the most common PPIs
Losec
Pariet
Nexium
what is the typical 1st line tx in triple regimen
Losec
Amoxicillan
Nexium
what is the typical 2nd line tx in triple regimen
Zantac
Amoxicillan
Biaxin
what is the normal course of an Abx in triple regmine
week - 10 days
what is the normal course of a PPI or H2Ra in triple regmin
weeks - months
when is sx used to treat PUD
if complications arise, usually do sx repair during endoscopy
