Inflammatory disease (GI) Flashcards
what are the inflm disorders of the Gi tract
diverticular disease
IBSyndrome
peritonitis
appendicitis
iBDisease
ulcerative colitis
Crohn's diseasewhat is diverticular disease
an (singular diverticulum or multiple divrerticula) which is an out pouching
from the book: diverticulosis is a conditon in which the mucosal layer of the colon herniates through the muscularis externa layer
incidence of diverticular disease
5-10% AT 45YRS
80% AT >85YRS
et of diverticular disease
diet-poor, low in fibre (this can occur d/t poor dentition and inability to chew salad etc)
inactivity (dec perfusion)
poor bowel habits such as constipation (inc intraluminal pressure will give the force to cause a herniation)
aging (old tissues perform worse)
patho-diverticular disease
the areas that vessels enter are normal weak points
the inc intraluminal pressure leads to mucosa herniating through muscularis externa and then to bowel protrusion
this occurs mostly within the sigmoid colon. (although it can occur elsewhere in the GI tract. Not in stomach. Gen in lg intestine)
there are often multiple diverticula at multiple sites
diff bet diverticulosis and diverticulitis
diverticulosis can progress to diverticulitis.
diverticulosis is made up of non-inflamed out pouchings (these are usually not inflamed and the patient is gen unaware they have it)
diverticulitis occurs when the out-pouchings are inflamed
mnfts of diverticulosis
asymptomatic
mnfts of diverticulitis
dull pain
nausea
vomiting
low grade fever
DNLV
DuNauloFever diversion…road trip?
how can fever dev int he absence of exogenous pyrogens
when a cell is damaged eg by an infection or otherwise it will rel endogenous pyrogens. When these damaged cells are consumed by phagocytes the phagocytes will rel pyrogenic cytokines(IL-1, IL6, TNF) which when at the hypothalamus induce PGE2 to bind to the hypothalamic receptors via cAMP. this changes the T set point causing shivering and vasoconstriction
tx of diverticular disease
address the et and risks
sx for obstruction or perforation (this is addressing complications)
IBS is
a GI motility disorder that has variable mnfts (symptomatic problems)
there is no obvious abnormality of structure or fx
et of IBs
unclear
they have triggers more than risk factors
linked to diet, stress, smoking, lactose intolerance
Patho of IBS
theory re CHO…
(notes from him talking…
polyols are sugar alcohols such as sorbitol. fructose is an example of a fermentable cho.)
theory: malabsorption of fermentable CHO and polyols?
processed by gut flora which leads to flatulence. this can lead to abdominal distension and then to pain
patho of IBS theory re innervation
altered CNS regulationj of GI motor and sensory fx?
the CNS is largely involved in gut motility among other things leading to a prob w gut motility
patho of IBS most likely explanation
molecular signalling defect for serotonin
serotonin mediates motility in the gut
it is involved in:
sensation (esp pain),
secretion (eg hormones)
perfusion??
(serotonin is a NTM. it could be a problem of synthesis, release, action, or degradation etc)
site of synth of serotonin
.
serotonin action and IBS mnfts
,
mnfts of IBS
- abdm discomfort and pain
- diarrhea and or constipation (major prob for pts may have diff leaving house)
- flatulence
- nausea
- mucoid stool (may be d/t serotonin which causes inc secretion of mucus)
D/C FlaMuN pain. the guy who works at the factory wears lots of DC and flames and everyones in emotional pain because of this. this manifests on his person
dx of ibs
-based on exclusion of organic disease
various labs and scopes
-presentation
what types of labs/diagnostics might be done for dx of ibs
(ruling out so includes lots eg infection, cbc, parasites, barium swallow, endoscopy to rule out upper gi poblem, colonoscopy)
tx of ibs
-based on severity and type
-avoid offending foods eg limit dairy
-dec stress
-drugs:
antispasmodics-to dec pain and diarrhea-PRN eg MODULON
antidiarrheal
constipation
abx are sometimes used w caution to ec normal flora
et of peritionitis
bacteria (esp e coli) or chemical irritation (such as HCL from stomach)
- offening agent enter abm cavity via
- perforating ulcer
- ruptured appendix
- PID
- several others
patho peritonitis
-agents impact peritoneum –inflm
-large str means that agent is easily spread and rapid absorption of toxins (into circ system d/t mesentery being highly vascularized)
-thick exudate forms (purulent and sticky)
seals perforation
localizes inflm
how des body compensate for peritonitis
dec peristalsis through CNS to limit motility to dec gut content to dec amount of chyme that leaves perforation
mnfts of peritonitis
-severe
(the vascular response will be lg d/t lots of vasculature)
-fluid shifts why?
-ileus (cessation of peristalsis) fluid and air retained
-inc pressure, inc fluid secretion
(the gut releases fluid, namely mucous when irritated)
(this can lead to distention, rupture and hyperemia that can lead to hypovolemia)
-altered perfusion
blood is shunted to site of inflm
-dyspnea d/t pain
baby Perry w too much fluid shifting about, he cant move (ileus) theres inc P and inc fluid secretion, hes out of breath d/t pain, perfusion gets changed and moves to site of inflm
tx of peritonitis
iv abx
- anti inflm meds
- fluids and electrolytes
- pain
- sx if indicated (eg for perforated colon to remove exudate)
appendicitis
acute inflm of appendix wall
appendix loc and str
it is a blind ended tube connected to the cecum (which is at the junction of the small and large intestine) found in the left lower quadrant (McBurneys point)
appendix fx
it harbours healthy gut flora, is involved in lymphatic and immune fx,
when does appendicitis peak?
when is it common?
peaks at 20-30yrs
common between 5-30yrs
et appendicitis
idiopathic
- fecalith (a hard fecal pellet) obstructs cecum?
- twisted appendix or bowel?
patho appendicitis
- appendix lumen obstruction leads to drainage from the appendix into cecum being blocked. This inc the intra luminal P (which causes appendix to inc secretions).
- this exceeds venous P leading to venous stasis->ischemia->necrosis->bacteria invade wall (of appendix)
what is complication of appendicitis
perforation (can lead to peritonitis)
mnfts of appendicitis
acute epigastric or periumbilical pain (referred pain)
- pain increases
- then colicky (or spasmodic) over 12hr
- localizes to RLQ (rebound pain. pain on release of palpation
- nausea (and sometimes vomiting d/t pain)
- inc temp and inc WBC (d/t inflm and possible infection)
(they will be gaurding-lying in fetal position. McBurneys is the midpoint between umbilicus and iliac crest)
dx of appendicitis
hx
px
ultrasound
CT?
tx of appendicitis
IV fluids (because the inflm creates exudates and a fluid shift. this isnt as bad as peritonitis)
- abx
- appendectomy within 24-48hrs
- if theres delay can result in perforation and peritonitis
IBD is
2chronic conditions
- ulcerative colitis
- Crohn’s disease
et IBD
genetic susceptibility (not monogenic) -environ trigger (usually bact or viral, in this case bacterial (complex trait) -IR against NORMAL gut flora (this isnt autoimmunity as the bact arent part of the body and there isnt a problem with MHC or HLA)
what causes the inflm of IBD
(tolerance for normal gut flora is lost. if bact attaches to normal cells of gut lining the IR will destroy the normal cell too-inflm)
skipped lesions are found in
crohns
what is a fistula
a tunnel that connects two str
what is a stricture
a constricted area
crohns vs UC table 37.1
k
crohns vs UC
k
crohns vs UC
f
which layer of tissue is most affected by Crohn’s
what else
initially the submucosal
all layers of wall an be afected
Crohn disease
loc
primarily affects terminal ileum but other areas can be affected
Crohn’s lesion type
skip lesions (cobble stone appearance)
what type of progression is Crohn disease
slow, nonaggressive progression
mnfts of crohn disease
- diarrhea (there isnt enough time to absorb nutrients etc leading to wt loss)
- intermittent abdm pain (caused by food in GI tract-> peristalsis)
- wt loss d/t dec absorptive surface (most lesions are in sm intestine) this leads to nutritional deficit
ulcerative colitis what tissues are involved
-how does it spread
mucosa of colon and rectum
-proximal spread/ascending spread
ulcerative colitis lesions
bleeding ulcers (affects blood vessels more than Crohn’s)
- thickened, inflamed
- edema (from exudate) & congestion
mnfts of ulcerative colitis
bloody diarrhea
- abdm cramping (intermittent pain like in Crohn’s)
- may have slight wt loss but only losing wt d/t diarrhea
dx of IBD
hx
px
exclude GI infection (its mnfts are similar to beginning of IBD)
sigmoidoscopy, colonoscopy, biopsy (youre looking for polyps etc
(IBD is chronic so you must manage progression)
tx of IBD
- based on severity (adjust diet)
- anti inflm eg sulfasalazine (+Abx to prevent bact from entering damaged wall. take abx for short time)
- steroids if non responsive (to sulfasalazine)
- immunomodulator eg methotrexate (to dec IR but not eliminate it)
- sx?
histology of GI tract
mucosa which contains epithelium, lamina propria, muscularis mucosae
epithelium (str squam or simple columnar)
lamina propria (loose areolar w capillaries and lymph nodules)
muscularis mucosae (makes folds to inc SA and dislodge food)
submucosa (dense irreg CT w blood and lymph vessels and follicles. Anchors and feeds epith)
muscularis externa (inner circular and outer longitudinal layers of sm muscle
serosa or adventitia (serosa eg visceral peritoneum. Adventitia=fibrous CT, anchors organ to surroundings)
names of str of small intestine in order from mouth
duodenum
jejunum
ileum
name of str of colon from ileocecal valve
cecum ascending colon transverse colon descending colon sigmoid colon rectum external anal sphincter
