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pathways > Inflammatory disease (GI) > Flashcards

Inflammatory disease (GI) Flashcards

1
Q

what are the inflm disorders of the Gi tract

A 
diverticular disease
IBSyndrome
peritonitis
appendicitis
iBDisease
       ulcerative colitis
        Crohn's disease
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2
Q

what is diverticular disease

A

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

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3
Q

incidence of diverticular disease

A

5-10% AT 45YRS

80% AT >85YRS

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4
Q

et of diverticular disease

A

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)

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5
Q

patho-diverticular disease

A

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

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6
Q

diff bet diverticulosis and diverticulitis

A

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

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7
Q

mnfts of diverticulosis

A

asymptomatic

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8
Q

mnfts of diverticulitis

A

dull pain
nausea
vomiting
low grade fever

DNLV

DuNauloFever diversion…road trip?

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9
Q

how can fever dev int he absence of exogenous pyrogens

A

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

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10
Q

tx of diverticular disease

A

address the et and risks

sx for obstruction or perforation (this is addressing complications)

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11
Q

IBS is

A

a GI motility disorder that has variable mnfts (symptomatic problems)
there is no obvious abnormality of structure or fx

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12
Q

et of IBs

A

unclear

they have triggers more than risk factors
linked to diet, stress, smoking, lactose intolerance

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13
Q

Patho of IBS

theory re CHO…

A

(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

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14
Q

patho of IBS theory re innervation

A

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

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15
Q

patho of IBS most likely explanation

A

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)

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16
Q

site of synth of serotonin

A

.

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17
Q

serotonin action and IBS mnfts

A

,

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18
Q

mnfts of IBS

A
  • 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

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19
Q

dx of ibs

A

-based on exclusion of organic disease
various labs and scopes
-presentation

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20
Q

what types of labs/diagnostics might be done for dx of ibs

A

(ruling out so includes lots eg infection, cbc, parasites, barium swallow, endoscopy to rule out upper gi poblem, colonoscopy)

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21
Q

tx of ibs

A

-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

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22
Q

et of peritionitis

A

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
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23
Q

patho peritonitis

A

-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

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24
Q

how des body compensate for peritonitis

A

dec peristalsis through CNS to limit motility to dec gut content to dec amount of chyme that leaves perforation

25
Q

mnfts of peritonitis

A

-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

26
Q

tx of peritonitis

A

iv abx

  • anti inflm meds
  • fluids and electrolytes
  • pain
  • sx if indicated (eg for perforated colon to remove exudate)
27
Q

appendicitis

A

acute inflm of appendix wall

28
Q

appendix loc and str

A

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)

29
Q

appendix fx

A

it harbours healthy gut flora, is involved in lymphatic and immune fx,

30
Q

when does appendicitis peak?

when is it common?

A

peaks at 20-30yrs

common between 5-30yrs

31
Q

et appendicitis

A

idiopathic

  • fecalith (a hard fecal pellet) obstructs cecum?
  • twisted appendix or bowel?
32
Q

patho appendicitis

A
  • 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)
33
Q

what is complication of appendicitis

A

perforation (can lead to peritonitis)

34
Q

mnfts of appendicitis

A

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)

35
Q

dx of appendicitis

A

hx
px
ultrasound
CT?

36
Q

tx of appendicitis

A

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
37
Q

IBD is

A

2chronic conditions

  • ulcerative colitis
  • Crohn’s disease
38
Q

et IBD

A 
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)
39
Q

what causes the inflm of IBD

A

(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)

40
Q

skipped lesions are found in

A

crohns

41
Q

what is a fistula

A

a tunnel that connects two str

42
Q

what is a stricture

A

a constricted area

43
Q

crohns vs UC table 37.1

A

k

44
Q

crohns vs UC

A

k

45
Q

crohns vs UC

A

f

46
Q

which layer of tissue is most affected by Crohn’s

what else

A

initially the submucosal

all layers of wall an be afected

47
Q

Crohn disease

loc

A

primarily affects terminal ileum but other areas can be affected

48
Q

Crohn’s lesion type

A

skip lesions (cobble stone appearance)

49
Q

what type of progression is Crohn disease

A

slow, nonaggressive progression

50
Q

mnfts of crohn disease

A
  • 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
51
Q

ulcerative colitis what tissues are involved

-how does it spread

A

mucosa of colon and rectum

-proximal spread/ascending spread

52
Q

ulcerative colitis lesions

A

bleeding ulcers (affects blood vessels more than Crohn’s)

  • thickened, inflamed
  • edema (from exudate) & congestion
53
Q

mnfts of ulcerative colitis

A

bloody diarrhea

  • abdm cramping (intermittent pain like in Crohn’s)
  • may have slight wt loss but only losing wt d/t diarrhea
54
Q

dx of IBD

A

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)

55
Q

tx of IBD

A
  • 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?
56
Q

histology of GI tract

A

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)

57
Q

names of str of small intestine in order from mouth

A

duodenum
jejunum
ileum

58
Q

name of str of colon from ileocecal valve

A 
cecum
ascending colon
transverse colon
descending colon
sigmoid colon
rectum
external anal sphincter

pathways (15 decks)

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