Irritable Bowel Syndrome/Diverticulitis Flashcards

1
Q

IBS

A

Defined by Rome III: recurrent abdominal pain/discomfort + improvement with defecation + onset associated with change in frequency and form of stool 3x/month

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2
Q

4 categories of IBS

A

irritable bowel + consitpation, irritable bowel + diarrhea, irritable bowel + mixed, unclassified

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3
Q

IBS epi

A

females>males, 5-20% in developed countries –> most commonly diagnosed GI condition

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4
Q

Why is IBS important?

A

no decrease in life expectancy but reduced QOL and high cost of health-care utilization/work absenteeism

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5
Q

Etiology of IBS

A

mixed: motility, visceral sensitivity, genetic, fecal flora, inflammation, food, psychosocial

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6
Q

What is the neuronal cause of visceral hypersensitivity?

A

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

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7
Q

What antibiotic can improve IBS without constipation

A

Rifaximin –> alters microbiome, thus changing IBS

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8
Q

What is post-infectious IBS?

A

increased risk of IBS after infections

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9
Q

What is SIBO?

A

small intestinal bacterial overgrowth –> fermentation –> tx of SIBO reduces IBS

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10
Q

In IBS-D, ___ is produced. In IBS-C, ___ is also produced.

A

hydrogen and methane

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11
Q

T/F Fiber can increase IBS symptoms

A

F–> tx for IBS as long as not fermentable or doesn’t breakdown into SFCA –> can increase motility

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12
Q

How do lipids cause IBS symptoms?

A

increase motility and sensitivity

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13
Q

T/F Gluten can cause symptoms in IBS patients with celiac disease?

A

T

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14
Q

Intestinal inflammation w/mast cells and lymphocytes are common in some patients with _____.

A

IBS-D and postinfectious IBS

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15
Q

How does intestinal inflammation cause mucosal permeability leading to IBS?

A

inflammation releases mediators that change tight junction proteins leading to outflow of antigens across intestinal wall –> increased activation of immunocytes + increased sensitivity and motility

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16
Q

Which genes are connected to IBS?

A

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

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17
Q

T/F early adverse life events can lead to IBS

A

T due to sustained neurological dysfunction

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18
Q

T/F IBS patients tend to have more anxiety, depression, phobia, somatization

A

T

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19
Q

What is a diverticulum?

A

sac like protrusion of colonic wall

20
Q

What is diverticulosis?

A

you’ve got diverticulas

21
Q

A typical colonic diverticulum is true/false

A

false –> does not have all layers of wall, just mucosa

22
Q

Congenital diverticuli are true/false

A

true –> have all layers

23
Q

What are the usual symptoms of diverticulosis?

A

usually asymptomatic

24
Q

Main colonoscopic finding in US?

A

diverticula!

25
Q

Western nations have left/right sided diverticuli

A

left –> acquired

26
Q

Asian nations have right/left sided diverticuli

A

right –> congenital

27
Q

Where do most patients have diverticulosis?

A

descending and sigmoid colon –> but uneven distribution in colon

28
Q

Etiology of diverticulosis

A

anatomic weakness, low fiber, nt’s, increased intraluminal pressure, disordered motility

29
Q

Point of anatomic weakness in bowel wall

A

points at which vasa recta penetrate circular muscle layer

30
Q

Law of Laplace

A

p = kt/R | P = pressure, K = conversion factor, T = wall tension, R = bowel radius

31
Q

Why is the sigmoid colon common for diverticulosis?

A

small radius = higher pressure a la laplace –> risk factor

32
Q

____ muscle reduces functional length of colon

A

longitudinal

33
Q

____ muscle controls peristalsis

A

circular

34
Q

What happens to muscle in diverticulosis?

A

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

35
Q

What collagen is deposited in diverticulosis?

A

collagen III due to MMP and inhibitor imbalance especially with age

36
Q

T/F segmentation is exaggerated in diverticulosis

A

T –> outpouchings of colon cause diverticula formation

37
Q

How does disordered colonic motility manifest in diverticulosis?

A

increased smooth muscle with age –> increase in segmental contraction + lower # of cajal cells = disordered contraction

38
Q

What NT changes occur in diverticulosis?

A

increased excitatory: serotonin + ACh
decreased inhibitory: NO, VIP

= increased motility and pressure

39
Q

3 factors in developing symptoms in diverticular disease

A
  1. diet (low fiber, high fat/meat)
  2. low physical activity
  3. obesity
40
Q

Symptomatic diverticular disease

A

inflamed diverticulum, segmental colitis (SCAD), symptomatic uncomplicated diverticular disease (SUDD

41
Q

Persistent GI symptoms from DD w/o overt macroscopic colitis or diverticulitis.

A

SUDD –> e.g. fecal stasis leads to abnormal metabolites and chronic inflammation

42
Q

Pathophysiology of diverticulitis

A

erosion of diverticular wall –> inflammation –> focal necrosis –> perforation
perforations:
1. contained = obstruction or fistula
2. not contained = peritonitis

43
Q

T/F DD can overlap with IBS

A

T –> similar constellation of causes and DD can lead to IBD in 10% of cases

44
Q

T/F there can be visceral hypersensitivity in DD

A

T –> post inflammatory increases neuropeptides and alterations in enteric innervation

45
Q

How does diverticular bleeding occur?

A

blood vessel exposed in luminal injury –> eccentric intimal thickening and thinning of media –> segmental artery weakness –> rupture into lumen