Irritable Bowel Synfrome Flashcards

1
Q

is a functional bowel disorder characterized by abdominal pain or discomfort and altered bowel habits in the absence of detectable structural abnormalities.

A

is a functional bowel disorder characterized by abdominal pain or discomfort and altered bowel habits in the absence of detectable structural abnormalities.

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2
Q

Clinical features:
affects all ages,
although most patients have their first symptoms
before age 45

A

Women are diagnosed with IBS two to three times

pain is a key symptom for the diagnosis of IBS

Rome IV criteria is more stringent, requiring abdominal pain to occur at a minimum of once a week and eliminates “discomfort” as one of the criteria

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3
Q

Supportive symptoms

not included diagnosis

A

defecation straining, urgency or a feeling of incomplete bowel movement, passing mucus, and bloating.

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4
Q

prerequisite clinical feature of IBS.

A

Abdominal pain

episodic and crampy, but it may be superimposed on a background of constant ache

s, malnutrition due to inadequate caloric intake is exceedingly rare with IBS.

Abdominal pain present only using the waking hours

nocturnal pain is a poor discriminating factor between organic and functional bowel disease.

Pain is often exacerbated by eating or emotional stress and improved by passage of flatus or stools.

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5
Q

Rome IV Diagnostic Criteria for Irritable Bowel Syndrome Recurrent

Criteria fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis.

A

Recurrent abdominal pain, on average, at least 1 day per week in the last 3 months, associated with ≥2 of the following criteria:

  1. Related to defecation
  2. Associated with a change in frequency of stool
  3. Associated with a change in form (appearance) of stool
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6
Q

Clinical manifestation
2. Altered bowel habits
most consistent clinical feature in IBS

First: episodic constipation—-> intractable
sense of incomplete evacuation,
:

A
  1. Predominant constipation: IBS-C
  2. Predominant symptoms is diarrhoea
    -stool volumes: less than 200ml: 33%
    IBS-D
  3. IBS-M: mixed

Nocturnal diarrhoea does not occur.

Bleeding is not a feature of IBS

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7
Q

Gas and Flatulence

IBS frequently complain of abdominal distention and increased belching or flatulence, all of which they attribute to increased gas.

A

Most IBS patients have impaired transit and tolerance of intestinal gas loads

with IBS tend to reflux gas from the distal to the more proximal intestine, which may explain the belching.

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8
Q

Upper GI symptoms:
20-50%: IBS complained with dyspepsia, heartburn, and vomiting IBS show a high incidence of abnormalities in the small bowel during the diurnal (waking) period

A

IBS show a high incidence of abnormalities in the small bowel during the diurnal (waking) period

Prevalence of IBS is higher among patients with dyspepsia (31.7%)

IBS 55.6% reported symptoms of dyspepsia

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9
Q

pathophysiolodgy of IBS

A
  1. Bile malabsorption
  2. Brain-gut interaction
    HPA axis
    Autonomic dysfunction
  3. Motility abnormality
    4.leaky gut dyes bios is
    5.visceral hypersensitivity
    6.pyschologi
    Anxiety/panic
    Depression
    Somatization
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10
Q

GI motor abnormality

-myolectrical an emoter

A

contrast, colonic motor abnormalities are more prominent under stimulated conditions in IBS

Increases rectosigmoid motor activity up to 3 hours after eating

  • prolonged distention-evoked contractile activity
  • rapid colonic transit and abdominal pain
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11
Q

Visceral hypersensitivity

-vesiral afferent dysfuction

A

frequency of perceptions of food intolerance is at least twofold more

  • post prandial pain has been temporally related to food entry into the caecum.
  • prolonged fasting in IBS associated with relief of symptoms

Lipids lower the thresholds for the first sensation of gas, discomfort, and pain in IBS patients

-postprandial symptoms: nutrient dependent exaggerated sensory component of gastroclolic response

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12
Q

Mechanisms of visceral hypersensitivity

A

(1) increased end-organ sensitivity with recruitment of “silent” nociceptors
(2) spinal hyperexcitability with activation of nitric oxide and possibly other neurotransmitters;
(3) endogenous (cortical and brainstem) modulation of caudad nociceptive transmission; and

(4) over time, the possible
development of longterm hyperalgesia due to development of neuroplasticity, resulting in permanent or semipermanent changes in neural responses to chronic or recurrent visceral stimulation.

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13
Q

Central neural dysregulation

A

shown that in response to distal colonic stimulation, the mid-cingulate cortex—a brain region concerned with attention processes and response selection—shows greater activation in IBS patients.

preferential activation of the prefrontal lobe, which contains a vigilance network within the brain that increases alertness.

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14
Q

Abnormal psychological features

A

Abuse is associated with greater pain reporting, psychological distress, and poor health outcome

posterior and middle dorsal cingulate cortex, which is implicated in affect processing in IBS patients with a past history of sexual abuse.

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15
Q

Postinfectious IBS

A

more commonly in females and affects younger rather than older patients.

Capylobacter, shigella, salmonella’s

Campylobacter infection who are toxin-positive are more likely to develop postinfective IBS

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16
Q

Immune activation and mucosal inflammation

A

peripheral blood mononuclear cells (PBMCs)

Mucosal Inflammation Some patients with IBS display persistent signs of low-grade mucosal inflammation with activated lymphocytes, mast cells, and enhanced expression of proinflammatory cytokines.

IL6,Il1b, and TNF

TRPV1 channels in the sensory neurons of the gut has been observed in IBS

shown increased intestinal permeability in patients with IBS-D
,

17
Q

Altered Gut flora

A

s, in general IBS patients had

decreased proportions of the genera Bifidobacterium and Lactobacillus and

increased ratios of Firmicutes:Bacteroidetes

Firmicutes is the dominant phylum in adults consuming a diet high in animal fat and protein

18
Q

Abnormal serotonin pathways

A

serotonin (5-HT)-containing enterochromaffin cells in the colon are increased in a subset of IBS-D patients compared to healthy individuals or patients with ulcerative colitis.

postprandial plasma 5-HT levels were significantly higher

Tryptophan hydroxylase 1 (TPH1) is the rate-limiting enzyme in enterochromaffin cell 5-HT biosynthesis,

19
Q

Approach to the patient with Irritable bowel syndrome

A

its diagnosis relies on recognition of positive clinical features and elimination of other organic diseases.

IBS: recurrence of lower abdominal pain with altered bowel habits over a period of time without progressive deterioration, onset of symptoms during periods of stress or emotional upset, absence of other systemic symptoms such as fever and weight loss, and small-volume stool without any evidence of blood.

major symptoms of IBS—abdominal pain,
abdominal bloating,
and alteration in bowel habits—are common complaints of many GI organic disorders, the list of differential diagnoses is a long one.

20
Q

Pain due to IBS:
Epigastric or periumbilical are must be differentiated from biliary tract disease, peptic ulcer disorder, intestinal ischemia, carcinoma of the stomach and pancreas.

A

Pain: occur mainly in the lower abdomen, the possibility of diverticula disease of the colon, inflammatory bowel disease (including ulcerative colitis and Crohn’s disease) and carcinoma of the colon must be considered.

Intestinal infestation: giardia lamblia

Diarrhoea: major complaint the possibility of lactase deficiency, laxative abuse, malabsorption, celiac spruce hyperthyroidism, inflammatory bowel disease and infectious arrhea..

21
Q

Diagnostic work up

A

Diarrhoea—: sigmoid colon biopsy— to rule out microscopic colitis.

Age more than 40: air contrast barium enema

Diarrhoea + increase gas: possibility of lactase deficiency, ruled out by hydrogen breath test or with evaluation after a 3-week lactose-free diet.

Celiac sprue: respond with gluten free diet

In patients with dyspepsia: upper GI radiographs or esophagogastroduodenoscopy

Post prandial right upper quadrant: ultrasound of the gall bladder

Laboratory features that argue against IBS include evidence of anemia, elevated sedimentation rate, presence of leukocytes or blood in stool, and stool volume >200–300 mL/d. These findings would necessitate other diagnostic consideration

22
Q

Treatment : irritable bowel syndrome:

A
  1. Patient counselling and dietary alterations
    - excessive fructose and artificial sweeteners such as sorbitol or mannitol

Diet: FODMAPs ( fermentable oligosaccharides, disaccharides, monosaccharides and polyols ( helpful in IBS patients)

-dietary fibre
Effective treatment for for IBS
Increase stool weight decrease
colonic transit time

Psyllium: produce less bloating and distension

20-30grams of total dietary and supplementary fibre per dAY.

23
Q

TREATMENT;

Antispasmodic: provide temporary relief for symptoms such as painful cramps related to intestinal spasm

A

postprandial pain is best managed by giving antispasmodics 30 min before meals so that effective blood levels are achieved shortly before the anticipated onset of pain

Belladonna alkaloids: ceros Tomis, urinary. Hesitancy, and retention, blurred vision and drowsiness.

Dicyclomine: lesser side effects

24
Q

Treatment: antidiarrheal Agents:
1. Opiate-based agents are initial therapy of choice for IBS D

painless diarrhea variant of IBS, small doses of loperamide, 2–4 mg every 4–6 h up to a maximum of 12 g/d, can be prescribed

A

antidiarrheal agent that may be used in IBS patients is the bile acid binder cholestyramine resin as up to 30% of IBS-D patients may have bile acid malabsorption

25
Q

Antidepressant drugs:
mood-elevating effects, antidepressant medications have several physiologic effects that suggest they may be beneficial in IBS

A

IBS-D patients, the tricyclic antidepressant imipramine slows jejunal migrating motor complex transit propagation and delays orocecal and whole-gut transit, indicative of a motor inhibitory effect.

serotonin reuptake inhibitor (SSRI) paroxetine accelerates orocecal transit, raising the possibility that this drug class may be useful in IBS-C patients

26
Q

Antiflatulence therapy:
Avoiding flatogenic foods, exercising, losing excess weight, and taking activated charcoal are safe but unproven remedies. A low FODMAP diet has been shown to be quite effective to reduce gas and bloating (see Low FODMAP Diet).

A

Simethicone: surfactants

Antibiotics: helps patients with bloating

Pancreatic enzymes reduce bloating,gas, and fullness during and high-calorie,high-fat meal ingestion.

27
Q

Modulation of Gut flora: (gut dysbiosis)

Antibiotics: neomycin 500mg twice daily for 10days was more effective than placebo at improving symptoms scores among IBS patients

A

Rifaximin: nonabsorbed oral antibiotics
550mg two times daily for 2 weeks

only antibiotic with demonstrated sustained benefit beyond therapy cessation in IBS patients

28
Q

Are non digestible food ingredients that stimulate growth and or activity o bacteria in the GI tract

A

Probiotics

29
Q

defined as live microorganisms that when administered in adequate amounts confer a health benefit on the host

A

Probiotics:
IBS patients found significant relief of pain and bloating with the use of Bifidobacterium breve, B longum, and Lactobacillus acidophilus species compared to placebo

30
Q

Low FODMAP diet:

FODMAPs are poorly absorbed by the small intestine and fermented by bacteria in the colon to produce gas and osmotically active carbohydrates

A

A diet rich in FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) often triggers symptoms in IBS patients

FODMAP: serve as nutrient for colonic bacteria and promote the growth of gram negative bacteria whic may induce mucosal damage.

Fructose and fractals induce IBS symptoms in a dose-dependent manner.

31
Q

Serotonin receptor agonist and antagonist

A
  • therapy for IBS-D
  • 5-HT3 receptors enhances the sensitivity of afferent neurons projecting from gut.

-induces rectal relaxation, increases rectal compliance and delays colonic transit.

Novel 5-HT4 receptor agonists such as tegaserod exhibit prokinetic activity by stimulating peristalsis

Novel %HT4 receptor agonist: tegaserod exhibit pro kinetic activity by stimulating peristalsis.
-tegaserod: accelerated intestinal and ascending colon transit.

Diarrhoea: major side effect. However, tegaserod has been withdrawn from the market; meta-analysis revealed an increase in serious cardiovascular events

32
Q

Chloride channel activators:
Lubiprostone: is a bicyclist fatty acid that stimulates chloride channels in the apical membrane in the intestinal epithelial cells.

A

Oral lubiprostone: effective management of patients with constipation-predominant IBS

Lubiprostone 8ug twice daily for 3 months than in those receiving placebo.

Major side effects: nausea, and diarrhoea

Lubiprostone is a new class of compounds for treatment of chronic constipation with or without IBS

33
Q

Guanylate cyclase-C agonist

A

Linaclotide
is a minimally absorbed 14-amino-acid peptide guanylate cyclase-C (GC-C) agonist that binds to and activates GC-C on the luminal surface of intestinal epithelium

linaclotide accelerates GI transit and reduces visceral nociception.

analgesic action of linaclotide appears to be mediated by cGMP acting on afferent pain fibers innervating the GI tract.

34
Q

For IBS-D patients, treatments include gut-acting pharmacologic agents such as antispasmodics, antidiarrheals, bile acid binders, and the newer gut serotonin modulators

For IBS patients with predominant gas and bloating, a low-FODMAP diet may provide significant relief.

A

IBS-C patients, increased fiber intake and the use of osmotic agents such as polyethylene glycol may achieve satisfactory results.

For patients with more severe constipation, a chloride channel opener (lubiprostone) or GC-C agonist (linaclotide) may be considered.

low FODMAP diet as the first line of treatment of IBS patients with moderate to severe symptoms.