Irritable Bowel Syndrome/Diverticulitis Flashcards
IBS
Defined by Rome III: recurrent abdominal pain/discomfort + improvement with defecation + onset associated with change in frequency and form of stool 3x/month
4 categories of IBS
irritable bowel + consitpation, irritable bowel + diarrhea, irritable bowel + mixed, unclassified
IBS epi
females>males, 5-20% in developed countries –> most commonly diagnosed GI condition
Why is IBS important?
no decrease in life expectancy but reduced QOL and high cost of health-care utilization/work absenteeism
Etiology of IBS
mixed: motility, visceral sensitivity, genetic, fecal flora, inflammation, food, psychosocial
What is the neuronal cause of visceral hypersensitivity?
excessive/prolonged excitation of afferent pathways resulting in neuronal sensitization anywhere in the neuronal pathway –> CNS dysregulation + abnormal stimulus increases perception of symptoms in IBS
What antibiotic can improve IBS without constipation
Rifaximin –> alters microbiome, thus changing IBS
What is post-infectious IBS?
increased risk of IBS after infections
What is SIBO?
small intestinal bacterial overgrowth –> fermentation –> tx of SIBO reduces IBS
In IBS-D, ___ is produced. In IBS-C, ___ is also produced.
hydrogen and methane
T/F Fiber can increase IBS symptoms
F–> tx for IBS as long as not fermentable or doesn’t breakdown into SFCA –> can increase motility
How do lipids cause IBS symptoms?
increase motility and sensitivity
T/F Gluten can cause symptoms in IBS patients with celiac disease?
T
Intestinal inflammation w/mast cells and lymphocytes are common in some patients with _____.
IBS-D and postinfectious IBS
How does intestinal inflammation cause mucosal permeability leading to IBS?
inflammation releases mediators that change tight junction proteins leading to outflow of antigens across intestinal wall –> increased activation of immunocytes + increased sensitivity and motility
Which genes are connected to IBS?
TNFS and IBS + TLR9 and post-infectious IBS, bile acid synthesis KLB and IBS-D, some neurotransmitters and cytokines, guanylate cycle C and obvi HLA DQ2/8
T/F early adverse life events can lead to IBS
T due to sustained neurological dysfunction
T/F IBS patients tend to have more anxiety, depression, phobia, somatization
T
What is a diverticulum?
sac like protrusion of colonic wall
What is diverticulosis?
you’ve got diverticulas
A typical colonic diverticulum is true/false
false –> does not have all layers of wall, just mucosa
Congenital diverticuli are true/false
true –> have all layers
What are the usual symptoms of diverticulosis?
usually asymptomatic
Main colonoscopic finding in US?
diverticula!
Western nations have left/right sided diverticuli
left –> acquired
Asian nations have right/left sided diverticuli
right –> congenital
Where do most patients have diverticulosis?
descending and sigmoid colon –> but uneven distribution in colon
Etiology of diverticulosis
anatomic weakness, low fiber, nt’s, increased intraluminal pressure, disordered motility
Point of anatomic weakness in bowel wall
points at which vasa recta penetrate circular muscle layer
Law of Laplace
p = kt/R | P = pressure, K = conversion factor, T = wall tension, R = bowel radius
Why is the sigmoid colon common for diverticulosis?
small radius = higher pressure a la laplace –> risk factor
____ muscle reduces functional length of colon
longitudinal
____ muscle controls peristalsis
circular
What happens to muscle in diverticulosis?
increased elastin deposition –> thickened taenia coli = highly contractile normal muscle + thickened circular muscle = luminal narrowing –> bowel division into segments/compartments
+
increased collage deposition –> increased rigidity –> decreased compliance/accommodation to increased pressure
What collagen is deposited in diverticulosis?
collagen III due to MMP and inhibitor imbalance especially with age
T/F segmentation is exaggerated in diverticulosis
T –> outpouchings of colon cause diverticula formation
How does disordered colonic motility manifest in diverticulosis?
increased smooth muscle with age –> increase in segmental contraction + lower # of cajal cells = disordered contraction
What NT changes occur in diverticulosis?
increased excitatory: serotonin + ACh
decreased inhibitory: NO, VIP
= increased motility and pressure
3 factors in developing symptoms in diverticular disease
- diet (low fiber, high fat/meat)
- low physical activity
- obesity
Symptomatic diverticular disease
inflamed diverticulum, segmental colitis (SCAD), symptomatic uncomplicated diverticular disease (SUDD
Persistent GI symptoms from DD w/o overt macroscopic colitis or diverticulitis.
SUDD –> e.g. fecal stasis leads to abnormal metabolites and chronic inflammation
Pathophysiology of diverticulitis
erosion of diverticular wall –> inflammation –> focal necrosis –> perforation
perforations:
1. contained = obstruction or fistula
2. not contained = peritonitis
T/F DD can overlap with IBS
T –> similar constellation of causes and DD can lead to IBD in 10% of cases
T/F there can be visceral hypersensitivity in DD
T –> post inflammatory increases neuropeptides and alterations in enteric innervation
How does diverticular bleeding occur?
blood vessel exposed in luminal injury –> eccentric intimal thickening and thinning of media –> segmental artery weakness –> rupture into lumen
