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Digestive > 30 - IBS and IBD > Flashcards

30 - IBS and IBD Flashcards

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
Q

Central sensitisation

A

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
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26
Q

Why may IBS patients experience symptoms and pain beyond the gut

A

May be convergence of gut innervation and somatic structure innervation at the spinal cord

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27
Q

How is central brain processing involved in IBS

A
  • 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
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28
Q

What is the spinal cord gate control theory

A

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

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29
Q

Hypervigilance

A

Brain focuses on processing unpleasant stimuli so it is more aware of the peripheral stimulus and more sensitised to the discomfort

30
Q

Effect of stress on IBS

A

Brain -gut communication is bi-directional

Brain and stress influences gut motor, sensory, secretory and immune functions of the GI tract

31
Q

What are the 4 ways IBS is treated

A 
conventional 
dietary 
natural 
lifestyle 
> no identifiable pathology so no medicine to specifically treat
32
Q

Conventional treatment of IBS

A
  • 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
Q

Loperamide

A

Is an anti-motility drug

34
Q

Why are tricyclic anti-depressants used

A

To block neurotransmitters and receptors of pain perception

35
Q

Dietary treatment of IBS

A

Dietary treatment is based on the concept of IBS as multiple food sensitivities
Diets based food associated symptoms

36
Q

What dietary plan is recommended for IBS and why

A 
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
Q

Polyol

A

Artificial sweeteners

38
Q

Natural treatment of IBS

A

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
Q

Lifestyle treatment of IBS

A

regular meals and unhurried
reduce stress
sleep
Psychological therapies like hypnotherapy aim to help cope with stress and relax

40
Q

What causes symptoms of IBS to improve

A
  • 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
Q

Genetic features of IBD

A
  • 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
Q

Are genetics more important in crohns or UC

A

Crohns (higher concordance in monozygotic twins)

43
Q

NOD2 gene

A

Increases risk of crohns

44
Q

Environmental contributions to IBD

A
  • 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
Q

What is the pathophysiology of IBD

A
  • 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
Q

Pathology of UC compared to CD

A

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
Q

Where would you see a cobblestone appearance and why

A

Crohns disease

Is not limited to mucosa but is transmural so can form fissures (deep ulcers NOT in UC) and is gut swollen

48
Q

Histology of UC compared to CD

A

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
Q

What is a granuloma

A

A granuloma is an area of inflammation made up of giant cells by the fusion of macrophages

50
Q

histological features of ulcerative colitis

A
  • 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
Q

How are CD and UC diagnosed

A

Both require a biopsy to be diagnosed

52
Q

Can both UC and CD cause blood in stool?

A

YES but not in IBS

53
Q

Clinical of UC compared to CD

A 
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
Q

Lab Tests of UC compared to CD

A

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
Q

Complication of ulcerative colitis

A

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
Q

Inflammatory clinical presentation of CD

A 
Colitis
> similar to UC get a diarrhoea with blood 
Ileitis
> abdominal pain 
> malabsorption > diarrhoea
57
Q

Strictures clinical presentation of CD

A
  • 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
Q

Fistulas clinical presentation of CD

A
  • abnormal connection between the gut and other organ
  • enterocutaneous fistula/enterenteric/rectovaginal/entercolic
  • can be caused by inflammation
59
Q

Perianal clinical presentation of CD

A
  • perianal abscess (next to anus)
  • perianal fistula (between rectum and surface of anus)
  • anal fissure (tear in anal membrane)
60
Q

Do you get complications of IBD outside of the gut

A

Yes in both Cd and Uc such as skin problems such as skin problems

61
Q

4 ways IBD is treated

A
  1. 5 - ASA/Aminosalicylate
  2. Steroids
  3. Immunosuppression
  4. Biologics
    > i.e. antibodies to TNF/inflammatory cytokines to settle inflammation
62
Q

Main way IBD is treated

A

5 - ASA
5 - aminosalicylates
Have mild inflam action

63
Q

When would you use surgery in IBD

A
  • Only really if medical treatment fails to resect diseased bowel (ileal resection or colectomy)
  • Or to treat complications like fistulas, obstructions, perforations, abscesses
64
Q

IBD or IBS: Common

A

IBS (1/20 vs 15000)

65
Q

IBD or IBS: older onset

A

Older less likely in older (20-40 common)

IBD can be young or old but less likely in old

66
Q

IBD or IBS: Just diarrhoea no alternating bowel habit

A

IBD tends to just have diarrhoea

IBS tends to have swinging bowel habit due to altered gut motility

67
Q

IBD or IBS: Bleeding

A

NO bleeding in IBS as not structural

Must be IBD (UNLESS bleeding is due to haemorrhoids from constipation and strain)

68
Q

IBD or IBS: Alarm signals

A

Not in IBS

May occur in IBD

69
Q

IBD or IBS: Blood test abnormalities

A

Normal in IBS

in IBD usually have abnormal blood tests (immune cells, neut, ferritin, inflamm markers, iron deficiency, B12)

70
Q

IBD or IBS: other abnormalities

A

IBD

Perianal, extra-intestinal manifestations

Digestive (24 decks)

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