Unit 1 Flashcards
what is diverticular disease
when the mucosa herniates via musclaris lt a non inflammed outpouching
what is the clinical term for an outpouching
diverticula
where are diverticula most common
sigmoid colon
what is important to remember about GI mucosa in diverticular disease
it is all intact
what is the percent incidence after age 80
85%
et/risks of diverticular disease
ageing
diet
poor bowel habits (all leading to constipation)
why do outpouchings occur in diverticular disease (patho)
weak points in wall where blood vessels enter that are normally tight, loosen with age
what happens to intralumanal P in diverticular disease
increased, lt inc strain on GI wall lt mucosia herniating thru muscularis externa
2 types of diverticular disease
diverticulosis
diverticulitis
diverticulosis
asymptomatic out pouchings of GI tract
diverticulitis
inflm that is problematic
diverticulitis mnfts
dull aching pain, low grade fever, nausea, vomiting
why do diverticulitis pts have fevers
endogenous pyrogens (cytokines -> interlukin 1 and 6) are released into blood stream resulting in fever
tx of diverticular disease
address ET/risks
sx for obstruction or perforation
IBS
intestinal mobility disorder related to peristalsis with no obvious patho
et of IBS
unclear, but risks and triggers are related to diet, followed y smoking, stress, lactose intolerance
general patho of IBS
alterted CNS regulation of GI motor and sensory fx
what is the first speculation of patho in IBS
ingestion of fermentable cho’s and polyols results in inability to digest by stomach -> content moving to LI causing normal flora to digest and create gas as a by product -> pain
eg of fermentable cho
fructose
eg of polyol
sorbitol
second speculation of patho in IBS
molecular signalling defect via seratonin, resulting in dysfx at the molecular lvl regarding seratonin
what is seratonin
NT
where is most seratonin produced
epithelial cells in the GI tract
what are the 4 normal fxs of seratonin
Motility - peristalsis
sensation - pain
secretion - mucous, H , enzymes
perfusion - dilation/constriction of vessels
what do problems at the molecular lvl involve
signalling, messengers
mnfts IBS
abdominal pain and discomfort
constipation/diarhea
mucoid stools
flatulence
can a pt have both constipation and diahrhea (not simultaneously)? how so?
its based on peristalsis and the trigger causing the problem.
what is the number one mnft/problem in ibs
constipation / diarhea / bowel habits
why may an ibs pt have mucoid stools
dt abn mucous sec / inc mucous sec dt seratonin dysfx
dx IBS
difficult to dx, work by exclusion to ensure its not an organic disease, Labs, scopes, presentation
labs done in IBS
cbc, lytes, parasites, stool sample, barium swallow
scopes done in IBS
endoscopy, colonoscopy
tx IBS
based on mnfts and sev, avoid offending foods, dec stress, drugs
types of drugs used to tx IBS
antispasmadics, antidiahreals, laxatives, abx?
fx of antispasmadic drug? eg
dec spasms and pain related to diahrea
modulon
fx of abx
may be used if normal gut flora is prolifferating too quicky dt inc synth of polyols and fremented chos by them
peritonits
inflm of peritonium
fx peritonium
serous memb that forms lining of abdominal cavity, composed of mesothelium and CT, keeps organs in place and attatches them to abdm strs
et of peritonitis
bacteria invading GI tract
chemical irritation
what may cause bacterial invasion of GI tract
perforation of GI str
what may cause chemical irritation of GI
peptic ulcer, HCl, bile, PID, ruptured appendix, colonoscopy, sx
how do infcts enter GI
via perforation, ulcer, or rupture
PID
infc that ascends up female reproductive system via infundibulum -> inc risk for peritonitis
How does the large str of the peritonium affect patho (2)
badly. 1) inc prolif of bact d/t its easy spread 2) richly vascularised area -> potential CVS absorption of toxins -> systemic infc
what exudate forms in peritonitis
thick, sticky, purulent
fx of exude in peritonitis (2)
1) creates a barrier -> dec spread + localizing infc
2) plugs perforation/seals hole in tract
what is the compensatory response by the CNS in peritonitis
causes SNS to limit peristalsis in attempt to dec amount of content which passes by the perforation in attempt to dec amount of content lost into peritonium
why may mnfts of peritonitis be severe
systemic mnfts are occuring as a result of local infc
mnfts of peritonitis
altered perfusion
dyspnea
fluid shift
why is altered perfusion a result of peritonitis
dt inc inflm + inflm vascular response -> blood shunting dt hyperemia and vasodilation
why is dyspnea a mfnts of peritonitis
inc pain on breathing dt inflamed peritonium placing pressure on diaphragm -> results in inc discomfort when diaphragm moves
why is fluid shift a mfnts of peritonitis
result of inc perm d/t vascular imflammatory response
In peritonitis, where does the fluid shift to
towards the site of inflm
tx for peritonitis
IV abx, anti imflm med, IV fluids, Sx, Pain med
why are iv fluids given in peritonitis
to replace and fix fluid shift and and lyte imbalance
what does Sx do in peritonitis
repairs tear or perforation causing entry of bact into peritonium
fx of appendix
may have a fx in immune response
appendicitis
acute inflm of appendix wall
what ages have inc prevelenace of appendicitis + peag age
5-30, 20-30
Et of appendictis
idiopathic with 2 theories
what are the 2 theories of ET of appendicitis
1) fecalith obstructs cecum or anywhere in appendix -> blockage
2) twisting of bowel or appendix -> constriction of appendix lumen
patho of obstruction of appendix
obstruction -> inc intralumenal P dt blocked mucous drainage -> pressure pressing outwards on appendix wall -> lumneal P > venous P
what happens when lumenal P is > then venous P
venous statsis
why is venous stasis bad
venous stasis -> no drainage of appendix wall -> no influx of arterial blood -> ischemia
what happens when there is ischemia in the appendix wall dt obstr
necrosis, wall is compromised and normal flora is allowed to invade -> inflm
What happens when there is twisting or constriction of appendix bowel
localized accumulation of appendix content -> increase in intralumanl P etc..
common complication of appendicitis
perf or ruputre of appendix -> peritonitis
early mnft of appendicitis
acute gastric or periumbilical pain accompanied by nausea
what is referred pain in appendicitis talking about
acute gastric or periumbilical pain that occurs at onset
how does pain change over the course of 12h in appendicitis
becomes colicky and spasmotic
spasmotic pain
pain that is constant with periods of inc intensity
After the pain is spasmotic, what term is used to describe the pain /what happens (appendicitis)
pain migrates to LRQ and is rebound pain / gaurded pain
gaurded pain
pt assumes fetal position in attempt to relax abdm m. and dec pain
where does the pain eventually localize in appendicitis (late stage)
mcburneys point
mc burneys point
midpoint between iliac crest and umbilicus
mnfts of appendicitis (not pain)
fever, inc wbc count, nausea and vomitting
why does nausea and vomitting occur in appendicitis
dt proximity of neural pathways to pain center in brain PLUS GI mnfts
Dx of appenditis
patent progession of pain via Hx and Px
US, CT?
Tx of appendicitis
IV fluid, abx,
appendectomy via sx
fx of IV fluid in tx of appendicitis
correct fluid and lyte imbalance
fx of sx in appendicitis
to remove appendix to avoid rupture/perforation
2 chronic disorders common in IBD
ulcerative colitis
chrons disease
Et of IBD
genetic susceptibility
environmental trigger
IR targeting against normal flora
characteristics of genetic suscpetibility in et of ibd
not a monogenic issue, unclear genetic abn
characteristic of environmental trigger in et of ibd
normally a bact infc “complex trait”
what is important to note about IR targeting against normal flora
this is NOT autoimmunity
why is targeting of normal flora by IR in IBD not autoimmunity
Bacteria are not considered self components, so their targeting is not autoimmunity. there is no change in MHC to target this
why does targeting of normal flora -> inflm in IBD
flora has developed symbyiotic relationship with cells in GI tract and flora may be attatched to these cells -> when IR kills flora, it also damages host cell -> inflm in GI
distribution pattern of chrons
skip lesions thru out SI and LI
distribution pattern of ulcerative
continuous lesions from distal to proximal starting at anus and rectum
type of inflm in Chrons
granulomatus
type of inflm in ulcerative
ulcerative and exudative (erosion of gut plus exudate formation
level of involvment in chrons
primarily submucosa
level of involvement in ulcerative
primarily mucosa
what is meant my level of involvmenet
which part of the gut lining is affected
areas of involvment in chrons
primarily terminal ilium, secondarily colon
areas of involvement in ulcerative
primarily rectum and left colon
in which IBDs is diahrea common
both
incidence of rectal bleeding in chrons
rare
incidence of rectal bleeding in ulcerative
common
incidence of fistual in chrons
common
incidence of fistula in ulcerative
uncommon
incidence of stricture in chrons
common
incidence of stricture in ulcerative
rare
incidence of perianal abcess in chrons
common
incidence of perianal abcess in ulcerative
uncommon
CA dev in chrons
rare
CA dev in ulcerative
common
progression of chrons
slower and not aggressive
mnfts of chrons
intermittent abdm pain
diahrea and inc BMs
wt loss
why does intermittent abdm pain occur in chrons
dt eating and peristalsis causing content to move past lesions -> pain
why does diahrea and inc BMs occur in chrons
dec absorp -> inc content being excreted
why is there wt loss in chrons
dt l/o SA in SI -> dec area for absorption dt inc amount of scar itssue-> dec absorption of nutrients -> nutrient def
visually, what does chrons disease look like or is described as
“cobblestone” apperance dt presence of linear ulcerations, edema, surrounded by inflm
what does the continious inflm in ulcerative colitis result in
thickening tissue -> inc exudate prod moving into gut lumen -> edema and congestion
mnfts of colitis
bleeding
frank blood in stool/bloody diarrhea
crampy pain + abdmn cramping
dec body weight
what can bloody diahrea end up resulting in
anemia
what is important to remember about crampy pain in ulcerative colitis
it may be presistant and no different then pain in chrons
how is dec body weight in ulcerative comparable to chrons
less weight is lost in ulcerative dt no lesions in SI occuring -> not as much SA for absorption is lost
how to dx chrons
hx and px, differential dx. sigmoidoscopy, colonoscopy, biopsy too look for IBD
Tx for IBD
depnds on severity,
nutrition (dietary mods to remove offendting foods)
drugs
sx
which drugs are most common for IBD (4)
Sulfasalazine
Abx
Steroids
Immunomodulatory
fx of sulfasalazine in IBD
anti inflm
fx of abx in IBD
leads to decreasing amount of normal flora to aid in dec inflm + prophylaxis, to prevent normal flora from entering GI wall.
when is abx in IBD given
only after immediate dx
fx of steroids in IBD
given for inflm if sulfasalazine doesnt work
which immunomodulatory drug is given in IBD
methotrexate
fx of methotrexate, and its fx specific to IBD
anti CA drug in inc doses, anti folate (prevents DNA replication and cell division) dec T cell agression in Dec doses
why do we use immunomodulatory vs immunosurpressant
immunosupressants cause too much T cell damage which is not the goal
what sx occurs if nescessary in IBD
in attempt to repair fistulas, constriction, drain ulcers, resection parts of bowel
