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30 - IBS and IBD Flashcards

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1
Q

Which of IBS and IBD is a structural abnormality and which is structurally normal but is a functional gut disorder

A

IBS - functional gut motility. Structurally normal

IBD - structural abnormality

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2
Q

What do I need to know?

A
  1. Concept of functional GI disease
  2. The mechanism for abdominal pain in irritable bowel syndrome
  3. The common symptoms for irritable bowel syndrome and management
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3
Q

Structural or functional more common in practice?

A

Functional gut disorders

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4
Q

What are function gut disorders thought to be due to?

A

multiple factors that impede on gut function incl

  1. Gut motility
  2. Visceral Hypersensitivity
  3. Brain-gut communication dysfunction
  4. Physcological factors i.e. worsens with anxiety
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5
Q

Why are functional gut disorders hard to diagnose?

A

No obvious pathology so no particular test. No biochemical abnormality, histological or radiological features. Is instead diagnosed of exclusion

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6
Q

What is the Rome Criteria?

A

Rome criteria is the criteria for the diagnosis of all functional GI disorders developed by experts of the Rome Foundation
Don’t strictly have to meet these criteria to be diagnosed with a functional gut disorder
Is more used in study and research than clinically

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7
Q

Where can function gut disorders affect?

A

any part of the gut

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8
Q

Where does IBS in particular affect

A

The SI and LI

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9
Q

4 examples of functional GI disorders?

A
  1. Globus
  2. Functional heartburn
  3. Functional dyspepsia
  4. Functional vomitting
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10
Q

2 examples of functional GI disorders in SI/LI

A

IBS
> abdominal discomfort and bloating associated with defecation and altered bowel habit. Symptoms normally improved after bowel motion
Functional abdominal pain
> no change in bowel habit
> recurrent/consistent abd pain NOT associated with defecation

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11
Q

What are the 2 classical symptoms of IBS?

A
  1. Swinging bowel habit

2. abd pain relieved with defecation

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12
Q

4 associated symptoms of IBS?

A
  1. urgency and feeling if incomplete evacuation
  2. passage of mucus
  3. abdominal bloating
  4. excess flatus
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13
Q

When may IBS occur

A

Post infection/GEnteritis (post-infective IBS)

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14
Q

What are the 8 alarm signals

A
  • older (40/50)
  • short history
  • weight loss
  • anaemia/iron deficiency
  • rectal bleeding
  • vomiting
  • nocturnal symtoms
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15
Q

How common is IBS and who do you usually see it in?

A

common - about 20% of people. More common in women. Early onset 20-30

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16
Q

What other non-specific associated symptoms do you also see in IBS?

A

These are not required for diagnosis but often occur
- fatigue
- Functional dyspepsia
- early satiety and post prandial fullness
- nausea
- back or headache
- urinary symptoms
- dysmennorhea
- palpitations
- poor sleep
Dont related to the gut suggesting issue is bigger to do with pain perception/brain-gut communication or disordered visceral sensitivity

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17
Q

Alarm signals

A
  1. Vomiting
  2. Elderly
  3. Sudden onset/short history
  4. Anaemia/iron deficiency (occult bleeding)
  5. PR bleeding
  6. Nocturnal symtoms
  7. Family history
  8. Weight loss
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18
Q

What 2 things contribute to IBS symptoms (pathophysiology)

A
  1. Altered gut motility

2. Visceral hypersensitivity

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19
Q

What does altered gut motility mean in IBS

A
  • swinging bowel habit
  • altered frequency and duration of contractions
  • transit time
  • exaggerated response to meal ingestion and stress
    i.e. exaggerated with diarrhoea reduced with constipation
    There is usually a predominant one over the other
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20
Q

What does altered gut motility/frequency and duration of contractions suggest

A

Abnormal signalling

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21
Q

What symptoms does altered gut motility cause?

A

Swinging bowel habit

i.e. alters frequency and duration of contraction, transit time, exaggerated response to ingestion and stress

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22
Q

Visceral Hypersensitivity

A
  • more sensitive to and find distension more painful at lower intensity
  • have more awareness and perception of distension meaning they have a lower threshold to pain
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23
Q

What 2 categories does visceral hypersensitivity fall into

A

Peripheral and central sensitisation

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24
Q

Peripheral Sensitisation

A

Problem in the gut

  • can be post infective IBS
  • previous inflammation can up-regulate the sensitivity of nociceptors leading to increased sensitivity to pain stimuli
  • also increases sensitivity to non-painful stimuli perceiving it as painful
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25
Central sensitisation
Brain - Peripheral sensitisation can leading to surrounding uninjured tissue to also become hypersensitive - this is why IBS patients can get pain beyond the gut as it may be the innervation of gut CONVERGING with the innervation of somatic structure at the spinal cord
26
Why may IBS patients experience symptoms and pain beyond the gut
May be convergence of gut innervation and somatic structure innervation at the spinal cord
27
How is central brain processing involved in IBS
- how the brain processes visceral sensation differs in IBS - different parts of brain activated - the differences in how the brain processes pain contributes to symptoms away from the gut
28
What is the spinal cord gate control theory
That the brain usually filters out SOME peripheral pain signals In IBS it is thought that when the pain from the periphery encounters these nerve gates in the spinal cord the signals aren't filtered and so all reach the brain
29
Hypervigilance
Brain focuses on processing unpleasant stimuli so it is more aware of the peripheral stimulus and more sensitised to the discomfort
30
Effect of stress on IBS
Brain -gut communication is bi-directional | Brain and stress influences gut motor, sensory, secretory and immune functions of the GI tract
31
What are the 4 ways IBS is treated
``` conventional dietary natural lifestyle > no identifiable pathology so no medicine to specifically treat ```
32
Conventional treatment of IBS
- fibre supplement (fluid uptake in stool) - can aggrevate some symptoms like bloating - laxatives - anti-motility drugs to counteract increased motility like loperamide - low dose tricyclic anti-depressants (neuropathy pain - block neurotransmitter signalling for pain perception)
33
Loperamide
Is an anti-motility drug
34
Why are tricyclic anti-depressants used
To block neurotransmitters and receptors of pain perception
35
Dietary treatment of IBS
Dietary treatment is based on the concept of IBS as multiple food sensitivities Diets based food associated symptoms
36
What dietary plan is recommended for IBS and why
``` Low FODMAP Fermented Oligosaccharides Disaccharides Monosaccharides And Polyols FODMAPs are fermentable saccharides/sugars. Bacteria break these down to cause symptoms of gas and distension Includes gluten due to it causing excess fermentation NOT allergy ```
37
Polyol
Artificial sweeteners
38
Natural treatment of IBS
i.e. probiotics Introduce bacteria normally present in gut Problem as only know by trial and error who these people are Results can be strain dependent
39
Lifestyle treatment of IBS
regular meals and unhurried reduce stress sleep Psychological therapies like hypnotherapy aim to help cope with stress and relax
40
What causes symptoms of IBS to improve
- confident diagnosis - knowing no structural abnormality and understanding the condition (absence of disease) - effect of stress and diet - reassured by investigations and pathology exclusions - symptoms will remain need to learn to manage
41
Genetic features of IBD
- increased risk with first degree but most patients do not have family history - many genes not fully known - NOD2 gene will increase of CD in the ileum - uncommon in certain ethnic groups (maori and pacific)
42
Are genetics more important in crohns or UC
Crohns (higher concordance in monozygotic twins)
43
NOD2 gene
Increases risk of crohns
44
Environmental contributions to IBD
- IBD is common in western and developed areas i.e. improved living conditions so less exposure and so tolerance of the immune system to enteric infections - smoking is a risk factor for Crohns and makes crohns harder to treat while smoking is a protective factor for ulcerative colitis
45
What is the pathophysiology of IBD
- not fully understood - disruption of integrity of epithelial barrier - dysregulation of the immune system causes an abnormal immune response and triggering of inflammation - some gut microbes are pathogenic and trigger IBD
46
Pathology of UC compared to CD
CD = occurs in any part of gut discontinuous inflammation transmural inflammation so starts as small ulcer > penetrates with fissuring into muscle layer mucosa appears swollen and with fissuring causes cobblestone appearance UC= only in LI continuous ulceration from rectum then proximally only mucosal inflammation diffuse and granular don't often get ulceration only in severe disease
47
Where would you see a cobblestone appearance and why
Crohns disease | Is not limited to mucosa but is transmural so can form fissures (deep ulcers NOT in UC) and is gut swollen
48
Histology of UC compared to CD
CD = transmural inflam across wall non-nectrotising granulomas (supports diagnosis not in UC also in TB) transmural fissures and swollen/edema mucosa causes cobblestone appearance looks like cracking of mucosa UC= mucosal inflam only and chronic inflam infiltrate incl plasma cells intestinal crypt distortion and branching and atrophy neutrophils invade the crypts forming crypt abscesses loss of goblet cells paneth cell metaplasia; seen in places normally not seen like colon severe diffuse, granular, grainy and bleeding in severe
49
What is a granuloma
A granuloma is an area of inflammation made up of giant cells by the fusion of macrophages
50
histological features of ulcerative colitis
- branching and atrophic crypts - inflam cell (plasma) and neutrophil invasion in crypts forming crypt abscesses - loss of goblet cells - paneth cell metaplasia (usually in SI not LI)
51
How are CD and UC diagnosed
Both require a biopsy to be diagnosed
52
Can both UC and CD cause blood in stool?
YES but not in IBS
53
Clinical of UC compared to CD
``` CD = Inflammatory stricturing fistulas perianal presentations ``` ``` UC = Diarrhoea with blood Frequent bowel motions and urgency Abdominal discomfort Fever, malaise, weight loss (alarm signals - do not occur in IBS) ```
54
Lab Tests of UC compared to CD
CD = - increase in inflam markers ESR/CRP, platelets, neutrophils - mild anaemia (due to bleeding) - increased ferritin (an acute phase protein) - iron deficiency due to long term bleeding (with or without anaemia) - only difference in a lab test for CD will be a deficiency in B12 and iron deficiency and fat malabs as affects SI (usually) UC= - increase in inflam markers CRP/ESR and neutrophils - mild anaemia - increased ferritin - prolonged occult bleeding can cause decreased ferritin.iron deficiency with out without anaemia
55
Complication of ulcerative colitis
Toxic Megacolon - in severe cases can get paralysis of the colon which stops peristalsis so get a build up of gas and stool causing distension and increased risk of perforation
56
Inflammatory clinical presentation of CD
``` Colitis > similar to UC get a diarrhoea with blood Ileitis > abdominal pain > malabsorption > diarrhoea ```
57
Strictures clinical presentation of CD
- strictures arise due to chronic ulceration in CD - irreversible scarring forms a stricture causes symptoms of bowel obstruction (symptoms initially due to the swelling/oedema - abdominal pain and distension - vomiting - bowels not passing or opening
58
Fistulas clinical presentation of CD
- abnormal connection between the gut and other organ - enterocutaneous fistula/enterenteric/rectovaginal/entercolic - can be caused by inflammation
59
Perianal clinical presentation of CD
- perianal abscess (next to anus) - perianal fistula (between rectum and surface of anus) - anal fissure (tear in anal membrane)
60
Do you get complications of IBD outside of the gut
Yes in both Cd and Uc such as skin problems such as skin problems
61
4 ways IBD is treated
1. 5 - ASA/Aminosalicylate 2. Steroids 3. Immunosuppression 4. Biologics > i.e. antibodies to TNF/inflammatory cytokines to settle inflammation
62
Main way IBD is treated
5 - ASA 5 - aminosalicylates Have mild inflam action
63
When would you use surgery in IBD
- Only really if medical treatment fails to resect diseased bowel (ileal resection or colectomy) - Or to treat complications like fistulas, obstructions, perforations, abscesses
64
IBD or IBS: Common
IBS (1/20 vs 15000)
65
IBD or IBS: older onset
Older less likely in older (20-40 common) | IBD can be young or old but less likely in old
66
IBD or IBS: Just diarrhoea no alternating bowel habit
IBD tends to just have diarrhoea | IBS tends to have swinging bowel habit due to altered gut motility
67
IBD or IBS: Bleeding
NO bleeding in IBS as not structural | Must be IBD (UNLESS bleeding is due to haemorrhoids from constipation and strain)
68
IBD or IBS: Alarm signals
Not in IBS | May occur in IBD
69
IBD or IBS: Blood test abnormalities
Normal in IBS | in IBD usually have abnormal blood tests (immune cells, neut, ferritin, inflamm markers, iron deficiency, B12)
70
IBD or IBS: other abnormalities
IBD | Perianal, extra-intestinal manifestations

Digestive (24 decks)

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