GI Pathophysio Flashcards
vitamin a deficiency
night blindness
bitot spos (squamous cell prolif)
corneal perforation
How to diagnose diverticulitis
clinical if mild
CT scan or ultrasound
epithelium of the stomach
simple layer of columnar epithelial cells
secrete mucus and bicarb
pits provide glands access to the lumen
symptoms of pancreatic exocrine insufficeincy
bulky foul smelling stool
oily residue in toilet water
irritant laxatives
castor oil, senna
cause irritation of the enteric mucosa/nerves –> water secretion –> softer stool and increased peristalsis due to increased volume
may cause abdominal pain, flatulents
bile acid deficiency
when bile salt pool is very low, get maldigestion of fat and fat soluble vitamins
from liver disease (low production) or ileal resection (low recycling)
trituration
first, peristalsis down through stomach
terminal antral contraction closes pyloris
allows mixing of foodstuff into small particles until 1-2 mm
3-4 hours
NSAIDs and ulcer formation
decrease mucin and HCO3 so HCl can touch the cell
injury to cell - HCl can get closer!
vitamin D
fat solumble
storage form = 25OH, active form 1, 25 OH
found naturally in very few foods (fortified and sun)
calcium-phosphorus homeostasis (break down bone if not enough)
bone metabolism
IBS
Rome criteria -
absence of detectable structural or biochemical abnormaility
abdominal pain
altered bowel habits (alternating between diarrhea and constimation)
abdominal pain is most universal!
IBS-C
IBS with constipation
how do you diagnose celiac disease?
high antibody levels to: TTG IgA, DPG (deaminated peptide)
abnormal small bowel biopsies
response to gluten free diet
consequences of bacterial overgrowth
unconjugate bile acids
use vit b12
treatment of pancreatic exocrine insufficiency
pancreatic enzyme supplements wiht food
viberzi
binds to opioid receptors in GI tract controling motility and hypersensitivity
types of glands in the cardia
branched and tortuous
mucus
endocrine
pancreatic exocrine insufficiency
maldigestion of fat, protein, carbs
limited amylase, lipase, proteases
from CF, chronic pancreatitis, pancreatic resection
need to lose >90%
pre-epithelial defense in the esophagus
lacks a definable surface mucus layer!
has saliva which contains mucins
surface squamous cells can not secrete bicarb! rel unprotected
esohageal peristalisis in smooth muscle
inhibition followed by excitation
gradient of increasing inhibition (latency gradient)
beri beri
B1 deficiency
dry - peripheral neruopathy
wet - CHF
vitamin d deficiency
bone demineralization
hypocalcemia, hypophosphatemia
B12 absorption
dietary intake (meat, dairy)
pepsin in the stomach cleaves protein from B12
secretion of IF by gastric parietal cells
bound to R protein
unbound - binds to IF in the intestine
in the ileum - special R and complex absorbed into blood
diverticular bleeding pathophysiology
eccentric intimal thickening and medial thinning
segmental weakening
rupture where vessels run over the dome of a diverticulum
usually abrupt and painless - 75% stops on own
erythromycin
primarily prokinetic
motilin receptor agonist
The main function of motilin is to increase the migrating myoelectric complex component of gastrointestinal motility and stimulate the production of pepsin. Motilin is also called “housekeeper of the gut” because it improves peristalsis in the small intestine and clears out the gut to prepare for the next meal.[7] A high level of motilin secreted between meals into the blood stimulates the contraction of the fundus and antrum and accelerates gastric emptying. It then contracts the gallbladder and increases the squeeze pressure of the lower esophageal sphincter. Other functions of motilin include increasing the release of pancreatic polypeptide and somatostatin[11]
uncomplicated diverticulosis
asymptomatic - incidental, increase fiber
symptomatic - bloating, constipation, passage of mucus, like IBS
bethanechol
prokinetic
muscarinic receptor agonist
Cholestyeramine (questran)
bile acid sequentrant, prevent reabsorption
bile acids, once complexed, are secreted in feces
lower plasma cholesteral
used to prevent diarrhea pst ileal resection
d-xylose test
for carb malabsorption
D-xylose = simple sugar, some absorbed and some excreted
If absorbed – some metabolized by liver and some excreted by kidney
If not absorbing – none in blood stream and none in urine
Fasting – empty bladder, blood draw
Drink solution of sugar water – 2 hours later, repeat bloodd draw and see if blood level went up properly
Collect urine over 5 hours and see if xylose is in there – if really low not absorbing properly and sign of absorption problem
sibship size and gastric cancer risk
higher risk of cancer in later bown
higher risk with brothers and sisters
early years of life affect health decades later
gastric motility of liquids
rapidly disperse through stomach and empty without delay
prokinetics
Prokinetics help strengthen the lower esophageal sphincter (LES) and cause the contents of the stomach to empty faster.
more gerd?
combined prokinetic/amtoe,etoc
mixed micelles
transport lipolytic products (mostly fA and MG)
hydrophilic part on outside
vitamin K
dietary from plants, synthesize by gut bacteria
essential to function of blood clotting factors
bulk laxatives
i.e. metamucil, citrucel
absorb water, increase in stool volume triggers stretch receptors and causes reflex peristalsis that propels bowel contents forward
safe, most physiologic
fiber laxatives
12 hrs to tdays to work
vegetable fibers
stimulant laxatives
derivatives of phenolphtalein
induce high amplitude propagated colonic contracts
appear to be safe!
rescue agents when no BM for several days
opiates
systemic antidiarrheals
slow peristalsis - allow increased water reabsorption
gastric motility of solids
lag phase then trituration
rate depends on nutrient content too (fat is slowest)
fundoplication
surgical repair for hiatal hernia
The important one is called a surgical fundoplication, where the stomach, the fundus of the stomach over here (black arrow) which was originally over here (lavender arrow) is wrapped around the LES and sort of adds to its pressure.
how to diagnose gastroparesis
EGD to r/o obstruction
scintigraphy = gold standard
IBS pathophysiology
genetic/social factors + food and stress lead to symptoms
pseudoachalasia
malignancy (gastric)
paraneoplastic
chagas
eosinophilic gastroenteritis
infiltrative process at LES
tissue transglutaminase
deamidates or crosslinks gliadin - increasing its affinity for receptors on WBCs
folate
DNA synthesis
pathogenesis of diabetic gastroparesis
chronic hyperglycemia –> neuropathic changes and dysfunctional innervation through the vagus –> delayed gastric emptying due to autonomic neuropathy
Transient lower esophageal sphincter relaxations (TLESR)
occur primarily postprandially (facilitate belching)
occur in healthy and GERD pts in the same amt
propriton of reflux related to TLESR is greater in patients w GERD1
Well, what’s happening is all of a sudden in these sort of recordings, we see that in certain patients, they get these transient relaxations that are not associated with a a swallow (points at blue arrow segment)
So the sphincter just relaxes on its own, it’s usually a very prolonged relaxation, and that if you noticed, can cause the esophageal acidity to go down for a long period of time after it’s already relaxed for awhile and the reflux bolus goes up, you try to swallow it back down, but even so you might get a prolonged exposure of the esophagus to acid.
Barrett’s Esophagus
in response to acid reflux normal squamous epithelium may be replaced by columnar epithelium of the specialized intestine type
1% chance of adenocarcinoma (increasing!)
serotonin
imp NT and gut signaling molecule
major modulator brain-gut communication
activates enteric neurotransmission to initiate peristalsis and secretion
selenium deficiency
cardiomyopathy
vitamin E
anti-oxidant
short bowel with SHORT ileal resection
bile salt diarrhea
bile acids are incompletely reabsorbed for circulation back to the liver
bile acid spillage into the colon is irritating causing a secretory diarrhea
Tx: bile acid resins
percent weight loss
(UBW - Actual BW)/UBW x 100
3 hypotheses of diverticuli
- altered colonic wall structure: weak pts in the colon wall where the vasorecta penetrate from the muscularis propria into the submucosa
- abnormal motility: normally pressures are equal through colon, but increased segmentation in diverticular colons –> increased intraluminal pressures –> predisposes to hernieation
- dietary fiber: less risk with more fiber! fiber increases colon diameter, bulks stool, prevents increased P
hydrogen breath test
to test for lactase deficiency
HBT – lactase maldigestion
Fasting – blow into tube and blow baseline hydrogen methane production, drink lactos and blow into the tube every 20 min for a few hours
If gas levels peak to certain pt – lactose is not digested and lactase is delivering a lot of gas
If symptoms also – they are lactose intolerant –
short bowel syndrome
severe malabsorption condition following extensive small bowel resection
post duodeal length less than 5 feet
prone to severe diarrhea and weight loss due to rapid transit, lack of intestinal surface area, bile acid spillage, residual disease (crohns)
causes:
adults - intestinal ischemia, crohns volvulus trauma
children – congenital
niacin
B3
fundic accomodation
swallow initiation - fundus undergoes vagally mediated (NITROUS OXIDE!) relaxation - as meal enters the stomach, tnic and phasic contractions are inhibited - 2-3x increase in gastric volume!
h pylori and esophageal disease
vitamin e deficiency
hemolytic anemia
neuro (ataxia, peripheral neuropathy, myopathy
if eye or vision problems?
vit A
zinc 9f night blindness
Treatment for SIBO
antibiotics
correct underlying cause
mucosal phase of digestion
brush border hydrolysis
transport into epithelial cells (enterocytes)
when abberent - malabsorption
reciporcal relationship between adenocarcinomas of stomach and esophagus
if oily scaling around nares?
riboflavin or zinc deficiency
treatment of IBS
mutlidiscplinary
education and reassurance
dietary (avoid exacerbations w lactose, low FODMAP diet)
stress management
meds
how to diagnose achalasia?
endoscopy (not swallowing)
barium swallow
manometry** gold standard
gliadin
one of two types of protein that are components of gluten in wheat
contains the toxic AA sequences
secretagoges
Amitzia
latest laxatives
stimulate net efflux of ions and water into the intestinal lumen
accelerate transit and facilitate defectatin
activates Cl channels on apical - Cl rich fluid secretion - softens stool, increases motility, promotes Pm
pantothenic acid
B5
HLA DQ2 and HLA DQ8
receptors
on WBCs bind gliadin fragments and trigger an inflammatory cascade
celiacs
cytokines –> more inflam cells –> tissue damage
**during this process abs against TTG and deaminated gliadin develop
adherence pedistal
h pylori forms with epithelial cell to insert proteins
Consistent with that is the fact that HP is very smart and understand human biology well
- Slide shows epithelial cell and HP that have been cocultured
- Epithelial cell has formed adherence pedestal [points to supporting structure at bottom of oval blob]
- Helical cell has instructed the cell to form the pedestal through polymerization of actin
colonic diverticulosis
sac like protrusion of the colonic wall
mucosa and submucosa herniate through the muscularis
intrinsic LES
smooth muscle
gastric sling fibers
So, remember the LES is sort of a complex apparatus
It’s made up of intrinsic components, so we have the smooth muscle layers of the lower esophagus coming down so that’s the longitudinal and circular muscle layers.
And then there’s also an extrinsic component which is primarily made up of diaphragm so when there is no hernia or no sort of anatomical defect, this diaphragm contributes to the tone of the LES.
symptoms of SIBO
gas/bloat
diarrhea
maybe B12 deficiency? Bacteria uses B12
treatment for lactase deficiency
limit lactose containing foods
use lactase supplements
esophageal cancer and cancer
adenocarcinoma!
vitamin c deficiency - clinical manifestations
swollen bleeding gums
loose teeth
petechiae
periungal hemorrhage
impaired wound healing
arthalgias, joint effusions
corkscrew hair
anemia
cause of achalasia
uncertain
autoimmune?
altered inhibitory innervation of smooth muscle
loss of peristalsis
failure of les relaxation
tricyclic antidepressents
IBS
inhibitory effect on gut - alleviate symptoms at a very low dose
*amitripyline - take at sub depression levels
IBS-M
constipation and diarrhea
the bowel disorders
IBS
functional diarrhea
functional constipation
inhibitory innervation in the esophagus
more distal
how do you diagnose pancreatic exocrine insufficiency?
fecal elastase level -
Stool test – elastase – if enough pancreatic enzymes are in bowel and going into stool
Stool test to measure amt in the stool
types of glands in antrum
endocrine
mucus
g cells (gastrin)
impedence-pH monitoring
place transnasally for 24 hours
can detect liquid, air, reflux
adds impedence data - detection of changes in ersistance - detects all liquid reflux events from stomach to esophagus
area postrema
has chemoreceptor trigger zone (CTZ) sensitive to many stimuli
diverticulitis
likely due to increased lumenal pressure and thickened particulate matter that causes wall erosion, inflammation, perforation
uncomplicated
complicated - abcess, fistula, peritonitis (LLQ pain, nausea, fever)
cobalamin
B12
h pylori induces what kind of cancer?
adenocarcinoma
deficiency if neurologic?
B (1, 12)
vit E
dopamine antagonists
antiemetic
i.e. prochlorperazine
have peripheral prokinetic effects –> increase motility of the GI tract –> increases rate of gastric emptying
caution in patients w parkinsons!
soluble fiber
undigested until it reaches the colon
includes pectins, guar gum
used to thicken diarrhea
anticholinergics
systemic antidiarrheals
increase intestinal muscle tone and peristalsis
lots of side effects
prostiglandins
increased mucus and bicarb secretion
increase mucosal blood flow
riboflavin
B6
manometry
primary tool to measure esophageal peristalsis
record intraluminal pressure!
biphasic of h pylori
cyclin D1
HP can affect host cell genes in cell cycle
•Diagram shows effect of helicobac on cyclinD1 expression
oThis is one target gene shown as an ex but there are many others
- When helicobac sees cells, it binds to cell, launch CagA appartatus, injects CagA, gets phosphorylated and interacts with MAP kinases (e.g. ERK1/2, p38, JNK)
- MAPK phosphorylate transcription factors that work upstream of important genes like cyclin D1 that affect cell cycle progression
This is another example of how HP is talking to human cells
chromium deficiency
glucose intoleance (high blood sugar)
peripheral neuropathy
anticholinergics
antiemetic
esp for vestibular and gi disorders
post absorptive phase of digestion
processing within enterocyte
transport into blood stream and lymphatics
conditions of maldigestion
impaired nutrient hydrolysis
lactose intolerance
pancreatc insufficiency
small bowel bacteria over growth
bile acid deficiency
insoluble fiber
passes through intestine mostly unchanged
includes lignin, cellulose
used to treat mild constipation
extrinsic LES
diaphragmatic crural fibers
anchored by phrenoesophageal ligament
So, remember the LES is sort of a complex apparatus
It’s made up of intrinsic components, so we have the smooth muscle layers of the lower esophagus coming down so that’s the longitudinal and circular muscle layers.
And then there’s also an extrinsic component which is primarily made up of diaphragm so when there is no hernia or no sort of anatomical defect, this diaphragm contributes to the tone of the LES.
if beefy red tongue?
any of the Bs! 2, 3, 12
folate, protein, iron
B vitamin deficiency clinical signs
cheilosis (swollen lips), angular stomatitis (scaly only around nose)
seborrheic dematitis
anemia
gluten
storage protein in wheat, rye, barley
rich in prolamine and glutamine which leads to incomplete digestion by intestinal enzymes
long peptide results which passes through the epithelial barrier and triggers an immune reaction in genetically susceptible individuals
symptoms of diabetic gastroparesis
early satiety
bloating
nausea and vomiting
occasional bezoar development (accumulated indigestable material)
Linzess
actiaves guanylate cyclase c receptor on lumenealsurface of intestinal epithelal cells - opens CFTR and Cl secretion happens
IBS-D
IBS with diarrhea
excitatory innervation in esophagus
more proximal
h pylori and ghrelin
more ghrelin without h pylori
copper deficiency
impaired bone density
microcytic anemia
small intestinal bacterial overgrowth (SIBO)
excess build up of bacteria in upper small bowel
bacteria deconjugates bile acids and leads to impaired fat processing and absorption
red flags for NOT IBS
weight loss
nocturnal
fam history of colon cancer
blood mixed w stool
recent abx
lactase deficiency
inadequate levels of lactase in BB
lactase levels are highest after birth and decline after weaking
without lactase, lactose is not broken down into glucose and galactose
undigested lactose pulls water into lumen (osmotic)
this lead to rapid transit into the colon - bacteria ferment lactose and generate gas
primary = congenital , asians, africans, mediterranian
secondary - infectious enteritis, celiac, ibd
gastroparesis cause
30% = long standing diabetes
30% idiopathic (post viral?)
collagen vasc disease
amyloidosis
harris benedict equation
energy requirements
functional esophageal disorders
heartburn
chest pain
dysphagia
globus
hiatal hernia
GERD associated
So you have the esophagus smooth muscle coming down here. This would be the intrinsic LES (black arrow) with longitudinal and circular muscle layers. But now it’s been displaced from the diaphragm. Since normally the diaphragm adds to its pressure, that makes it inherently low pressure here (at the LES). Not only that, you have acid production happening right here directly (lavender arrow) and you can see that that might make it a little more easy to have acid coming up
A hiatal hernia (this is not a great picture of that), but it’s essentially when part of the stomach pushes up through the diaphragm and displaces the LES smooth muscle portion from the esophagus, from the diaphragm and sort of causes the whole apparatus to be a little bit separate and now you have acid production coming right here above the diaphragm and it can more easily come up.
NSAID ion trapping
wak acids!
once ionized, NSAIDs remain water soluble and “trapped” inside cell
factors in early life that can contribute to IBS
abuse
maternal deprivation
GI infections
abx
microbiome
early: diff factors cause development of abnormalities in ENS, visceral sensation, brain gut interactions, mental health
later: common environmental triggers like food and stress
tissue injury in celiac
increased intraepithelial lymphocytes
crypt hyperplasia
villous blunting
thiamin
B1
functional gastrointestinal disorders
multidetermined disorders
composite factors effect everything
gut mucosa, microflora, ENS, extrinsic neural connections, signalling brain and sc
treatment of achalasia
*decrease P in LES (gravity promotes emptying)
- pharma (botox)
- dilation of LES/surgical myotomy (cut through muscle)
- POEM - balloon tipped catheter
vitamin A
retinol
vision, immune function
osmotic laxatives
i.e. golytely (colo prep)
hypertonic agents draw fluid into lumen by osmosis and cause diarrhea
may cause electrolyte defects
effect in 3 hrs
laxatives
production of a soft formed stool over a period of 1 day or more
propmt fluid evacuation of the bowel - more intense
for constimation (pain, decreaseamt of strai, pre-exams)
retching
labored rhythmic respiratory activity and abdominal contractions that usually precede vomiting
builds up P gradient for vomiting
treatment of vomiting
treat complications (replace Na, water, K)
identify and treat underlying cause if possible
symptomatic relief
preventative measures (cancer therapy)
antihistimines
i.e. meclizine
esp for vestibular disorders
antiemetic
CCK
triggered by dietary fat in duodenum
- chyme entering duodenum causes enteroendocrine cells of the duodenal wall to release secretin but FATTY PROTEIN induces cck
- cck and secretin enter blood stream
- upon reaching pancreas, cck induces secretion of pancreatic juice (enzyme rich) - secretin causes more HCO3
GERD triggers
large meals
fatty spicy acid foods
bending, stooping, lying down
frequency of reflux related symptoms varies widely
lifting, staining, strenuous activities
adsorbants
pepto!
anti-dairrheal
coat the gut wall
bnd to causative bugs or toxins and permit elimination
treatment of compilcated diverticulitis
abscess
need to be drained and resect
selective serotinin RAs
esp to prevent chemo-induced nausea and vomiting
iron deficiency
facilitates oxygen delivery to tissue
deficiency - microcytic anemia
zinc deficiency risk and symptoms
at risk if chronic diarrhea
symp: scaly red rash around nose, mouth, eyes, groin
diarrhea (viscous cycle)
poor wound healing
impaired immune
decreased night vision
altered taste
treatment for short bowel syndrome
antidiarrheal medications
nutritional support - dietary interventions
complicated cases could require intestinal transplant
causes of SIBO
stasis!
from impaired motility or structural factors
Stasis – slow motility (structural, things not moving) – post surgery, connection sit that’s a pocket
scintigraphy
gastric emptying - gold standard for gastroparesis
solid/liquid emptying by radioloabeled meal
measure every 15 min for 4 hours
retention of >10% of solids at 4 hours = diagnosis
conditions of malabsorption
**impaired mucosal absorption of nutrients
loss of SA (celiac, small bowel syndrome, radiation), impaired lymph transport
PUFA
omega 6 and omega 3
lineoleic and lineolenic
essential FA can’t be made
treatment of gastroparesis
correct nutritional issues/electrolte problems
glucose control (if diabetic)
consider meds
gastroparesis in diabetcs
commonly have aberrant fundic accomodation
associated w dyspepsia and bloating
regurgitation
effortless movemeent of gastric contents toward the mouth without characteristic motor and autonomic changes seen w vomiting
types of glands in fundus
parietal
chief
endocrine
mucus
vitamin c
collagen synthesis, wound healing
riboflavin
B2
diverticulosis epidemiology
age related! almost all in older people
left sided in western
right sided in asia and africa
short bowel with long ileal resection
bile acids are so poorly absorbed htat the liver can’t synthesize enough to keep levels adequate
leads to fat maldigestion and malabsorption
restrict fat intake in diet
supplement with MCT oil
lubricant laxative
i.e. stool softener (colace), mineral oil
lubricates and softens stool
retards water reabsorption
works in 6-8 hrs little laxative effect
lowers surface tension of stool allowing water to enter and softening!
antispasmodics
anticholinergics
given based on the presuption that pain is due to intestinal spasm 0 minimally effective
Bentyl, LEvsin
pellagra
B3 deficiency - dermatitis, diarrhea, dementia
hyperpigmentation without uv exposure
GERD progression
normal
inflammed
baretts
dysplasia
adenocarcinoma
So this slide I’ll get back into a little bit later, just to give an overview of what reflux disease can progress into.
So, when you have a normal esophagus like in the video it should be looking sort of whitish, we say pearly white, the epithelium should be stratified squamous, and then, as acid starts to comes up into the esophagus over time, you can get the development of what’s called esophagitis. I’ll have another little video later, looking at that. And that’s really when your defense against acid in the esophagus is overwhelmed by the amount of reflux of acid up from the stomach and you can get esophagitis. On endoscopy it will look like this with sort of erosions and redness (erythema) coming out (pointing to second picture from left) And microscopically, there’s just a little more acid going through the layers.
Over time that acid reflux esophagitis we think is really the next step into going into Barrett’s esophagus. Now what is Barrett’s esophagus, Barrett’s is when the actual squamous mucosa starts changing, it’s called metaplasia and we’ll get into that in detail a little bit later. But the mucosa essentially becomes specialized into intestinal metaplasia. So, it becomes columnar and starts looking almost like the small intestine
After awhile, with prolonged acid in the esophagus with Barrett’s, the cells can become dysplastic which really is the next step into cancer.
So classically, you know, what we think is with acid reflux over time there’s a chance the patients can go from normal to esophagitis, to Barrett’s to dysplasia and then finally adenocarcinoma.
quantitative fecal fat test
for fat malabsorbtion
start 100g fat diet 2-3 days before study and continue through study
collect stool over 72 hours
if >7 g of fat in stool per day
5-HT Agonists
Tegoserod
accelerates gastric emptying and small bowel transit
for constipation dominant IBS - side effect is mild diarrhea
only if no response to fiber or laxatives
abdominal pain in IBS
visceral nerves affected
pain is diffuse and poorly localized
acid pocket
reservoir from which reflux originates after a meal
lag phase - food sits in fundus - why some more prone to GERD
increase reflux if closer to esophagus
can differ in patietns
treatment of uncomplicated diverticulitis
clear liquid diet
antibiotics
antiemetics
anti-vomiting
dopamine antagonists
serotinin antagonists
tricyclic antidepressants
Schilling test
assess cause of B12 deficiency
- oral B12 and intramuscular B12 - asses absorption by measuring urinary excretion over 24 hours - if low proceed to part 2 to see if it’s due to lack of IF
- labeled B12 is given with IF - if urinary excretion is normal - the patient has perniscous anemia (IF deficiency)
- give vit b12 and antibiotics - if normalizes, bacterial overgrowth is cause
- give B12 and panc enzymes - if normalizes pancreatic insufficiency is the cause
celiac disease
autoimmune where gluten triggers an immune raeaction that damages the small intestinal lining
functional gastroduodenal disorders
dyspepsia
nausea
vomiting
functional anorectal disorders
defectation disorders
fecal incontenance
anorectal pain
most common causes of peptic ulcer disase
h pylori
NSAIDs
GERD alarm symptoms
dysphagia
bleeding
weight loss
chest pain
gastric slow waves
always present, regular electrical pattern (produced by ICC!)
propigate circumerentially and migrate toward pylorus
do not lead to contractions by themselves! contractions occur on crests of slow waves
max contractions is directly related to slow wave frequency
deficiency if joint pain/weakness?
vit c
complication of achalasia
aspiration pneumonia
esophageal cancer risk (squamous - stasis esophagitis, adeno - GERD after LES disruption)
CagA
h pylori
HP produces protein called CagA and has type 4 secretion system used to export CagA and other materials from HP and directly inject into epithelial cells
- CagA has tyrosine phosphorylation domains that are recognized by host cell kinases like Sarc and Abl
- Phosphorylated protein [blue blob labeled Y-P] has many different activities within epithelial cells
- HP has whole repertoire of CagA or no CagA that signal the host in different ways
gastric lag phase
most solids stay in proximal stomach for 30-60 min
contractions then get food toward antrum
features of achalasia
incomplete relaxation of LES causes functional obstruction of esophagus
until hydrostatic P > LES P
dysphagia liquids/solids
difficulty belching
weightloss, CP, heart burn
5-HT antagonists
**diarrhea predominant IBS!
receptors on ENS sensory neurons
slow colonic transit and increase colonic compliance
reduce intestinal sensitivity to distention
types of unsaturated fats
MUFA - omega 9
PUFA - omega 6 and omega 3 (lineoleic and lineoenic) - essecntal FA and can’t be made
octreotide (sandostatin)
mimis somatostatin
inhibits secretion of gastrin, cck, glucagon, gh, insulin, secretin
reduces secretion offluids and motility
luminal phase of digestion
intraluminal substrate hydrolysis by various enzymes
maldigestion when abberant!
Nucleus tractus solitarius
may serve as central pattern generator for vomiting and taking in input via area postrema
then project to various motor nuclei in the vomiting reflex
