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Flashcards in GI INFLM Deck (47):

What is diverticular disease?

3 Types?

• Diverticular disease refers to the mucosal layer of the colon herniating through muscluaris externa layer (like a pouch) Often multiple diverticula and sometimes multiple sites

3 Types include
diverticulosis, diverticular bleeding, and diverticulitis

Diverticula (pl) Diverticulum (singular)


Prevalence of Diverticular Disease?

• (5-10% > 45yrs) AND (80% > 85yrs) have Diverticular disease


Etiology/RIsk Factors of DD

• Poor diet, not well balanced (specifically low fibre)
• Inactivity
• Poor bowel habits (specifically constipation)
• Ageing


What areas of the colon might be most effected in DD?

• Effects Normal weak points near areas of blood vessel entry

Also common in areas of high intra luminal pressure (sigmoid colon is common)


What is the trigger for herniation in DD?

• Accumulated gut content increases intra luminal pressure causing mucosa layer herniating through muscularis externa layer causing a bowel protrusion

(i.e constipation)


If a diverticulum develops near a blood vessel, what complication might arise?

• If problem arises near vessel entry, damage will lead to reduced blood flow to area, also potential increase risk of bacterial growth/invasion


Diverticulosis VS Diverticulitis

(Key difference and MNFTS)

• Non inflamed out pouchings
o Aysymptomatic

• Inflamed out pouchings
o Dull pain, nausea, vomiting, low grade fever


What is it called if a diverticulum is cut off from the rest of the gut



Tx for Diverticular Disease

• Focus on ET and risks (diet, exercise, bowel habits)
• SX for complications of obstruction or perforation


What is IBS?

a functional GI disease is order characterized by a variable combination of chronic or recurrent intestinal symptoms not explained by structural or biochemical abnormalities.

Major issue is the symptoms
• GI Motility Disorder
• MNFTS are Variable (mild to debilitating)
• No obvious abnormality of structure or function


Etiology of IBS

Etiology is unclear.
• Sometimes linked to diet, stress, smoking, lactose intolerance

IBS often includes a search for triggers


3 possible pathologies for IBS?

• Malabsorption of fermentable CHO (carbohydrates) and polyols (sugar alcohols) ex. Sorbitol. Unabsorbed then pass to colon where they are processed by gut flora causing flatulence

• Alteration of CNS regulation of GI motor and sensory fx

• Molecular signaling defect for serotonin


How might serotonin be related to IBS MNFTS?

• Serotonin actions and IBS MNFTS have parallels

o Serotonin facilitates perfusion, secretions, motility and pain and the GI tract is main site of synthesis



• TEXT: Hallmark is abd pain relieved by defecation and an associated change in consistency and frequency of stools

• Diarrhea AND/OR constipation
• Abdm discomfort and pain
• Flatulence (common caused by bacteria processing carbs), nausea
• Mucoid stool (irritated gut will inc mucous production, not generally beneficial)


DX of IBS?


• Generally largely based on pt presentation
o Work up is not precise, Dx by exclusion and MNFTS

• Requires exclusion of organic disease (large number of potential labs and scopes)

o Endoscopy (Upper GI- through mouth as far as duodenum)
o Colonoscopy (lower GI tract)
o Sigmoidoscopy (similar to colon, but not as far, simpler, less prep)


Non pharmaceutical TX IBS

• Based on severity, type and triggers
• Avoid offending foods (identify triggers and eliminate)
o Works for mild to moderate IBS

• Reduce emotional stress


Pharmaceutical tx of IBS

Abx WHY?

• Drugs only in severe cases
o Anti-spasmodic (modulon)
o Antidiarrheal/ or laxative
o Abx with caution (i.e. when necessary, short term, specific low dose)
• ABX may control numbers of normal flora to rebalance concentrations


What is peritonitus

• Inflm of peritoneum


Most common etiology of peritonitis?

•Bacterial (esp. E Coli) or chemical irritation (bile, Hydrochloric acid) of the peritoneal serous membrane from contents that have escaped GI tract



Offending agent enters abdm cavity via?

o Perferated ulcer
o Ruptured appendix
• Pelvic Inflm disease PID (bact enter through vagina, uterus, Fallopian tube, ova to ABD cavity
o Colonoscopy (inotrogenic)


What sort of exudate is present during peritonitis?

Thick and sticky exudate

Why thick?
Ahmed says thickness simply d/t to str and location


Pathogenesis of peritonitis

Two disadvantages of peritoneal inflm?

• Peritoneum is large structure allows easy spread across broad area
• Mesenchyme heavily vascularized allowing for rapid absorption of toxins


Two advantages to the thick exudate?

o Thick exudate forms
• Limits spread of bacteria (localization)
• Seals perforation


What is ileus?

refers to the cessation of peristalsis

• CNS limits GI motility during peritonitis (compensatory action and is intentional)


Three Key MNFTS of Peritonitis?

• Fluid shift (electrolyte imbalance)
o Ileus, fluid and air retained, Inc intra lumina pressure (GI), inc fluid sec in the gut (mucous)

• Alt perfusion
o Blood shunted to site of inflm

• Dyspnea
o Pain cause pt to limit breathing movements (larg infm abd strc)

NOTE- Can be severe leading to shock d/t volume of fluid involved


Tx for peritonitis?

• IV Abx
• Fluids and electrolytes
• Anti-inflm
• Sx if indicated


What is Appendicitis?

• Acute inflm of appendix WALL


Which age group are most at risk of appendicitis

• Peaks 20-30yrs but common in 5-30yrs


What is the etiology of appendicitis?



Two Theories of appendicitis etiology

Sometimes apparent on post-mortem, but not always

o Fecalith (hard small fecal pellet) obstructs cecum (opening to appx)
o Twisted appendix or bowel


Pathophysiology of appendicitis

• Appendix lumen obstruction -> drainage into cecum blocked -> inc intra luminal pressure (as mucous secretion continues)-> exceeds venous pressure (of veins in walls, close veins) -> venous stasis (no blood return, blocks blood in)-> ischemia -> necrosis -> bact invasion of appendix wall


What is the major complication of appendicitis?

Perforation (of an inflm bag of angry bacteria in your abdomen potential for peritonitis)


How will pain MNFTS over time in appendicitis?

Other MNFTS?

• Acute epigastric or periumbilical pain (referred pain)
• Pain increases
• Then colicky pain over 12 hrs (spasmotic, starts/stops)
• Localizes to LRQ (rebound pain, pt will be guarding)
• Ends with Mcburney point (Halfway along a line between iliac crest to umbilicus)

May also see some:
• Nausea
• Inc Temp and WBCs


Dx of appendicitis

• Hx and Px
• Ultra Sound
• CT


Tx of appendicitis

• IV Fluids
• Pain MNGMT
• Abx
• Appendectomy within 24-48 hrs
o Delay may end with perforation and peritonitis


Name 2 chronic conditions under the umbrella term IBD

Table 37-1

• Ulcerative colitis (lesion restricted to large intestine and continuous)
• Crohn disease (lesions found in both small and large intestine, not continuous- AKA skip lesions)


Basic Etiological components of IBD?

• Complex trait
o Genetic susceptibility (no specific gene)
o Environmental trigger (bacterial infection)


How is the IR involved in IBD?

o IR against normal gut flora
• Normally normal flora is tolerated by IR
• IN this case the IR targets normal flora
• These bacteria are not just in the lumen, but also in the lining of the gut (IR causes inflm and damage in lining)


Is IBD a kind of autoimmunity?

o This is not autoimmunity, because flora are not self components, but foreign components that are normally in body


Describe regions affected, lesion type and progression of Crohn's disease

FIG 37-7

• Primarily affects terminal ileum
o Other areas possible
• Primarily affects submucosa
o all layers possible
• Granulomatous skip lesion, lesion takes on cobblestone pattern
• Slow non-aggressive progression


MNFTS of Crohn's

• Diarrhea
• Intermittent abdm pain
• Weight loss (decrease in absorptive surface area -> nutritional deficiency


Describe regions affected, lesion type and progression of ulcerative colitis

• Primarily involves mucosa of colon and rectum
• Proximal spread from rectum
• Continuous lesion
o Bleeding ulcers
o Thickened and inflm and harden
o Edema and congestion


Describe MNFTS of Ulcerative colitis

• Bloody diarrhea
• Abdm cramping
• Some Weight loss (less so then crohn’s, but pain and GI irritability limits intake over long term)


Dx strategies for IBD

• Hx and Px
• Exclude Gi infections
• Sigmoidoscopy, colonoscopy, biopsy


What is the tx for mild IBD?

1rst and 2nd line tx for more severe cases?

• Very mild: diet manipulation might be enough)

• 1rst line- Anti inflm (eg Sulfasalazine) w/ short course of Abx

• 2nd line – steroids if not responsive


What other pharmaceutical tx might be affective at controlling progression of the disease? IBD

immunomodulator medication such as methotrexate (anti folate)

NOTE- Med reduces DNA and cell division. Also used in higher doses in cancer treatments


In what situations might Sx be required for IBD Tx?

Ulcer repair, fistula, drainage, resecting problematic section