Flashcards in GI INFLM Deck (47):
What is diverticular disease?
• 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)
• Poor bowel habits (specifically constipation)
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
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
• 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
MNFTS of IBS?
• 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
• 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
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
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
• 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?
• 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:
• Inc Temp and WBCs
Dx of appendicitis
• Hx and Px
• Ultra Sound
Tx of appendicitis
• IV Fluids
• Pain MNGMT
• Appendectomy within 24-48 hrs
o Delay may end with perforation and peritonitis
Name 2 chronic conditions under the umbrella term IBD
• 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
• 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
• 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