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Life Maintenance > Diarrhoea and IBS > Flashcards

Diarrhoea and IBS Flashcards

1
Q

Diarrhoea

A

a condition of excessively frequent and loose bowel movements
(>300g/24 hours)

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2
Q

Malabsorption

A

imperfect absorption of food material by the small intestine

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3
Q

What activates pancreatic proteolytic enzymes?

A

Trypsinogen

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4
Q

Stomach secretions

A

HCl, intrinsic factor, pepsinogen, gastrin

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5
Q

Gallbladder secretions

A

Bile (almost a litre)

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6
Q

Pancreatic secretions

A

HCO3, amylase, lipase, trypsinogen, CCK (Cholecystokinin)

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7
Q

Small intestine secretions

A

disaccharidases, peptidases

somatostatin

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8
Q

Anus secretions

A

Stool ~200g

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9
Q

Where do we start to absorb vitamins and nutrients?

A

Duodenum

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10
Q

What is absorbed in the duodenum?

A

Water soluble vitamins (active absorption)
Fat soluble (passive absorption)
Ca, Fe, An (increase by ascorbic acid, decrease with phytates)

Polysaccharides, proteins and fats

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11
Q

What is absorbed in jejunum?

A

Magnesium

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12
Q

What is absorbed in the ileum?

A

2ndary Bile acids, vit B12

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13
Q

What is absorbed in the large colon?

A

Na, Cl, water, SCFAs

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14
Q

What are the causes of diarrhoea?

A

Osmotic (non-absorbable solute)

Secretory (impaired electrolyte transport)

Exudative (intestinal mucosal damage)

Motility (increased transit)

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15
Q

Where are most sugars, proteins and fats absorbed?

A

Most polysaccharides, proteins and fats are digested and absorbed within the upper 200cm of the small intestine. Site of absorption depends on meal composition. Meat and salad absorbed high in the jejunum, while milk and doughuts are absorbed more distally, after a large amount of water has been secreted.

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16
Q

What are osmotic causes of diarrhoea?

A

Deficiency in digestive enzymes
Lactulose
Magnesium salts
Sorbitol

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17
Q

What are secretory causes of diarrhoea?

A

Bacterial endotoxins
Bile salts
Laxatives
Hormone producing tumours

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18
Q

What are exudative causes of diarrhoea?

A 
Infections
IBD
Coeliac diseaase
Irradiation
Ischaemia
Colon cancer
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19
Q

What are motility causes of diarrhoea?

A

Irritable bowel syndrome
Thyrotoxicosis
Autonomic neuropathy (DM)
Drugs

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20
Q
A
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21
Q

What do you want to find out from a patient’s history when diagnosing diarrhoea?

A

HISTORY OF PRESENTING COMPLAINT

Time course and severity
Impact of fasting on symptoms
Volume and consistency of stools
Floating stools
Bloody stools 
Nocturnal symptoms

Constitutional symptoms

  • Anorexia/weight loss
  • Fever
  • vomiting
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22
Q

What could we find from past medical history, social and family history that could help in diagnosing diarrhoea?

A

PMH:
childhood diseases
IBD
previous GI surgery

SH/FH:
foreign travel
contacts w similar symptoms
dietary factors (milk intolerance?)
ethnicity
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23
Q

Causes of diarrhoea: clues on examination

A

General - ?ill, shock, dehydration, pyrexia, anaemia, weight loss
hands, eyes, mouth, skin, joints, lymph nodes, oedema

CVS/RS - pulse, BP, etc.

Abdomen - distension, scars
tenderness, rebound, guarding
inflammatory masses, bowel sounds

PR/Epsilon - anus, anal canal, rectal mucosa, ?blood/pus, stool
rectal biopsy

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24
Q

Investigations of diarrhoea

A 
Blood tests:
FBC, ESR
U&E, LFT, CRP
Vit B12 and folate
Iron studies
TFT
Coeliac serology

Stool tests:
M,C and S
Elastase
Calprotectin

Functional tests:
Hydrogen breath tests
Schilling test

Imaging:
Barium studies/USS
CT/MRI

Endoscopy:
OGD with D2 biopsies
Colonoscopy
Capsule endoscopy/SBE

Gut hormone profile

Urinary catecholamines

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25
Q

Irritable bowel syndrome

A

IBS is defined as a “Functional” GI disorder, i.e. a disorder of gut–brain interaction.

These disorders are classified by GI symptoms related to any combination of the following:
motility disturbance
visceral hypersensitivity
altered mucosal and immune function
altered gut microbiota
altered central nervous system processing.

About 20% of adolescent/adult Westerners have symptoms consistent with IBS

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26
Q

Rome IV Criteria for IBS diagnosis

A

Recurrent abdominal pain, on average, at least 1 day/week in the last 3 months, associated with two or more of the following criteria:

  • Related to defecation
  • Associated with a change in frequency of stool
  • Associated with a change in form (appearance) of stool.

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

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27
Q

IBS management

A
  1. investigations + reassurance
  2. diet
  3. lifestyle advice
  4. medication for symptom relief:
    - anti-spasmodics
    - -mebeverine
    - -peppermint oil
  5. drugs to alter intestinal transit
    - opiates/loperamide
    - Laxatives
  6. probiotics
  7. anti-depressants
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28
Q

Coeliac disease

A

‘an inflammatory condition of the small intestinal mucosa, that is most marked proximally, and which improves morphologically when gluten is removed from the diet’

Inherited auto-immune condition
CD strongly associated with HLA-DQ2 genotype (95%)
likelihood of 1st degree relative having CD 10-15%

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29
Q

Gluten

A

Gluten is a general name for the proteins found in wheat (wheatberries, durum, emmer, semolina, spelt, farina, farro, graham, KAMUT® khorasan wheat and einkorn), rye, barley and triticale – a cross between wheat and rye. Gluten helps foods maintain their shape, acting as a glue that holds food together.

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30
Q

Coeliac disease autoantibodies

A
  • anti-gliadin
  • anti-reticulin
  • anti-endomysial
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31
Q

Coeliac disease UK prevalence

A

Prevalence probably M=F. but incidence higher (x2) in F (present during pregnancy and childbirth/feeding and because of fertility or menstrual problems).

GP study in Oxfordshire, screening of patients with anaemia (30 new CD patients identified (previously 8 on books)

Previously thought of as childhood disease, but now incidence increasing in adults and decreasing in children (better weaning and many commersial baby foods and milk gluten-free)

Adults usually diagnosed between 30 and 40, but increasingly now between 50 and 60.

Increased incidence almost certainly due to diagnostic phenomena

~150 patients at any one time in an average DGH

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32
Q

Histology for symptomatic, asymptomatic and latent coeliac disease

A

Symptomatic CD (positive histology)

Asymptomatic CD (positive histology)

Latent CD (negative histology)

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33
Q

Coeliac disease presentation: childhood vs adult

A 
Childhood:
Failure to thrive/short stature
Diarrhoea/steatorrhoea
Vomiting (50%)
Abdominal pain/distension
Adult:
Adults
Fatigue (80-90%)
Anaemia (85%)
Microcytic
Macrocytic
Diarrhoea/steatorrhoea (75-80%)
Weight loss
Mouth ulcers
infertility
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34
Q

Coeliac disease diagnostic criteria for adults

A

4 intestinal biopsies

abnormal mucosa on gluten*
b) improvement on GFD ( 3 - 6 months) #

       * Histological abnormality may be minimal (eg increased IEL only).
        # Mucosal healing may take 2 years - or remain incomplete.
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35
Q

What happens to villi in CD?

A

In untreated coeliac disease, villi become inflamed and flattened. In some cases, they can even disappear. This is called villous atrophy. When the gut is damaged in this way, it means the body can’t absorb all the nutrients from food properly.

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36
Q

Diseases associated w CD in adults

A
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37
Q

Dermatitis herpetiformis

A

Itchy blistering skin eruption which affects knees, elbows, buttocks and back

Complicates 2-5% of CD
prevalence 1:20,000 in UK
onset age 15-40 years
M>F
improved by GFD
diagnosis confirmed by granular IgA at dermo-epidermal junction of un-involved skin
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38
Q

Coeliac disease treatment

A

Gluten exclusion
-no food containing wheat, rye barley or ?oats

dietary supplements
-iron, folic acid, Ca, vitamin B12

bone abnormalities

hyposplenism

information and support

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39
Q

Why CD patients need a gluten free diet?

A
  • Amelioration of symptoms
  • reduction in risk of osteoporosis
  • reduction in risk of associated malignancies
  • reduction in risk of associated autoimmune diseases
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40
Q

Coeliac disease follow up

A

6 monthly OPA

  • (repeat small intestinal biopsy after 1st 6 months)
  • blood tests
  • symptomatic assessment
  • nutritional assessment
  • dietary compliance

close monitoring during pregnancy

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41
Q

Management of poor response/relapse CD

A

Important to check

  • dietary compliance
  • is the diagnosis correct?
-other co-incident disease
eg:
ulcerative jejuno-ileitis
microscopic colitis
malignancy
lymphoma
SB carcinoma
oesophageal/colonic carcinoma
42
Q

What is IBS?

A

chronic, relapsing, immunologically mediated
disorders (ulcerative colitis and Crohns) that are collectively referred to as
inflammatory bowel diseases (IBD)

43
Q

Which two conditions genetically overlap with many loci in common with IBS?

A

Crohn’s disease

Ulcerative colitis

44
Q

Ulcerative colitis

A

Chronic inflammatory disease of unknown aetiology, only affects colon

Presents with: Diarrhoea with blood and mucus

Systemic (extra intestinal) features if extensive and/or severe

Exacerbations and remissions

15-20% of attacks are ‘severe’

45
Q

Types of ulcerative colitis

A

Proctitis and distal colitis - only affects rectum

Left sided colitis - left side of colon

Pancolitis - affects all of large intestine

46
Q

What is the treatment for the different types of UC?

A

Proctitis: 5-ASA suppositories

Distal colitis: 5-ASA foam enema
L sided colitis: 5-ASA liquid enema

Extensive/pancolitis: topical Rx PLUS oral Rx

47
Q

Crohns disease

A

Chronic granulomatous inflammatory disease

Affects any part of the GI tract from mouth to anus

Commonest site ileo-colonic

Crohn’s colitis behaves similarly to ulcerative colitis
Minority of colitis cases indeterminate

48
Q

Protective and causative differences between UC and Crohn’s?

A 
UC:
smoking preventative
appendicectomy protective
8% concordance monozygotic twins
pANCA +ve 75%
Crohns:
smoking causative
appendicectomy NOT protective
67% concordance
pANCA negative, ASCA positive 86%
49
Q

UC vs Crohn’s presentation

A 
UC:
Bloody diarrhoea
Mucus
Mucosal and submucosal
Continuous disease
Association with PSC
Crohns:
Bloody diarrhoea
Mucus
Mucosal and submucosal
Continuous disease
Association with PSC
50
Q

UC vs Crohn’s pathophysiology

A 
UC:
Granular, friable mucosa
Pseudopolyps
Acute and chronic inflammation
Muscularis and serosa normal
Reduction in goblet cells, many crypt abscesses
Crohns:
Transmural
Submucosal oedema
Lymphoid aggregation and fibrosis
Apthous ulceration
Granulomas (eg sarcoid/TB)
51
Q

UC microscopic features

A

Architectural:
Crypt distortion
Decreased crypt density
Villous surface

Inflammatory:
Heavy diffuse transmucosal lamina propria cell increase
Diffuse basal 
Mucin depletion
Paneth cell metaplasia
52
Q

Crohn’s microscopic features

A

Architecture
Normal/irregular/villous
Crypt atrophy
Distorted,dilated, branching crypts

Inflammatory:
Basal plasmacytosis
Increase cells in basal third LP (round cells.

Specific:
Epitheliod granuloma
Basal giant cells
XS histiocytes in LP

53
Q

Problems UC and Crohn’s can cause in other parts of the body

A
54
Q

How is musculoskeletal affected by UC and Crohn’s?

A

Affects up to half of UC/Crohn’s patients
Arthritis - sero-negative spondylo-arthropathies
More common in colonic than small bowel dis
More common in Crohn’s colitis than UC
More common in pan-UC than left sided

Type 1 – pauciarticular- (less than 5 joints affected) – associated with disease activity
Type 2 – polyarticular, independent of disease activity

Treatment – NSAIDs/sulphasalazine

55
Q

Osteoporisis risk

A 
Common in patients with IBD
Corticosteroid use
Reduced physical activity
Inflamatory-mediated bone-resorption
Ca/vit D malabsorption
Poor intake (lactose intolerance)
Fracture risk 40% higher than general population
56
Q

Dermatological impact of UC/Crohn’s

A

2-34% of IBD pts
EN and PG most common
Psoriasis, apthous stomatitis, Sweet syndrome
EN – painful palpable nodules (F>M, CD>UC), mirrors disease activity
PG – usually shins , adjacent to stoma, pathergy
1-10.5% UC pts, 0.5-20% CD

57
Q

Hepatobiliary and pancreas (HPB) impact of UC/Crohn’s

A 
PSC (primary sclerosing cholangitis)
Cholelithiasis
Portal vein thrombosis
Drug-induced hepatotoxicity
Drug-induced pancreatitis
58
Q

PSC (primary sclerosing cholangitis)

A 
Inflammation, stricturing and fibrosis intra and extra-hepatic bile ducts
75% have coexisting UC (5% of UC)
5-10% have CD (2% of CD)
Pancolitis>left sided UC
30-59yrs
M:F 2:1
Think – raised ALP
33% raised ANA
80% raised ANCA

PSC RF for cholangiocarcinoma
12-15% of pts undergoing liver transplantation for PSC
Increased colorectal cancer risk

59
Q

Cholelithiasis

A

Crohn’s with ileal disease
Interruption of EHC of bile acids
Bile acid malabsorption

60
Q

Pancreatitis in IBD

A

Common side effect of azathiopurine and 6-mercaptopurine

61
Q

Ocular manifestations of IBD

A

0.3-5%
Less common in isloated small bowel disease
Episcleritis – can parallel intestinal activity – treat bowel disease- may need topical steroids
Scleritis – can impair vision – more severe – may require systemic steroids/immunosuppresion
Uveitis – assoc with joint/derm manifestation
F:M 4:1

62
Q

Renal/pulmonary manifestations of IBD

A

Nephrolithiasis
obstructive uropathy
Fistulisation
6-23%

Sulphasalazine – ILD
Pulmonary Embolus

63
Q

Acute colitis

A

Symptoms of colonic inflammation irrespective of cause of inflammation:

  • bloody diarrhoea
64
Q

Assessment of colitis

A

History
Features of toxicity: patient wellbeing, pulse rate, temperature, abdominal tenderness, abdominal distension,
Blood investigations ESR and CRP, Hb, white cell count,platelet count, albumin
Abdominal X ray

65
Q

Pharmacological treatment of ulcerative colitis

A 
5-Amino-salicylates (5-ASAs)
Azathioprine
Oral steroids
Intravenous hydrocortisone
Ciclosporin
Infliximab
66
Q

Severe colitis (Truelove and Witts criteria)

A

Truelove and Witts criteria:

6 bloody stools daily+  one or more of:
temp >37.8 C
pulse >90 per minute
Haemoglobin <10.5 g/dL
ESR >30 mm/h
67
Q

Diagnosing acute severe colitis

CASE:
18 year old boy
Admission to hospital with 3 weeks of bloody diarrhoea
Tired, lethargic
Bowel frequency 15/day, getting up at night time
Overweight, but losing weight

What do you do?

A 
DDx:
I.B.D.
Ischaemic colitis
BehÇet’s
Drug related exacerbations of UC: NSAID’s			cocaine, amphetamines
Drugs: nicorandil

Bacterial infection? (Salmonella, CMV colitis, Clostridium difficile, Ecoli?)

Day 1:
Bloods (FBC, U/Es, CRP, LFTS, CRP/ESR, also Mg + lipid profile), 
AXR, 	
Stool cultures, Stool O.C.P., 
C difficile toxin, 
Sigmoidoscopy and biopsy
REFER TO GASTROENTEROLOGIST

Blds – Hb 90g/dl, ESR 75, K 3.0, Alb 28, plts 540
HR 90, BP 95/40 temp 37.5

Now initiate treatment:
i.v. Hydrocortisone 100mg q.d.s.
Correct electrolytes
DVT prophylaxis
 Can eat and drink normally
Avoid opiates
68
Q

Truelove and Witt’s classification

A
69
Q

Management for acute severe colitis

A 
Daily bloods (correct electrolyte imbalance)
Stool chart
LMW heparin (VTE prophylaxis)
Avoid - 	opiate analgesia
			NSAID’s
			Anti-cholinergics
I.V.	Hydrocortisone
No role for bowel rest
No role for antibiotics in uncomplicated disease
70
Q

Factors predicting outcome in severe UC

A
71
Q

By day 3 of managing acute severe colitis you must have:

A

Stool culture results
Corrected electrolytes (especially Mg)
Colonic biopsy results
Gastroenterologists ready to decide on treatment escalation

72
Q

Toxic megacolon

A 
Daily abdominal x-ray
Toxic megacolon (megacolon toxicum) is an acute form of colonic distension				-  characterized by a very dilated colon 		- accompanied by abdominal distension, and 	 often fever, abdominal pain and shock

Very bad sign – call the surgeons

73
Q

What does severe colitis treatment escalation depend on? What are your options?

A

Depends on: Age, severity, “colitis history”, pre-flare up therapy, patients wishes

Options: cyclosporin, infliximab, surgery

74
Q

Cyclosporin

A

Calcineurin inhibitor
Blocks activation of pro-inflammatory mediators
Rapid onset with i.v. dosing
High oral bioavailability

Effectiveness:
Response rate 80-90%
30-47% colectomy rate at 6-39 months in responders
Avoidance of colectomy at 5 years in 55-70%

75
Q

Infliximab

A

Anti TNF biologic drug

Main use is in Crohn’s disease

Increasing evidence of use in UC

76
Q

Clostridium difficile

A

C difficile + IBD –> Colectomy rate 20%

C diff can mimic and precipitate IBD flares

IBD treatment may precipitate deterioration of C diff colitis

C diff enteritis more problematic in IBD patients

77
Q

When would you use surgery in IBD patient and what surgical interventions would you do?

A

When patient is no longer responding to medications, perforations or severe bleeding

Options:
Colectomy and ileostomy (ilium taken out and temporary stoma bag)

Then second procedure to restore continuity of intestines with anus

78
Q

Main causes of diarrhoea: Inflammation

A

INFLAMMATION:
1. Infective causes: gastro-enteritis / enterocolitis
- bacterial – eg Shigella, Salmonella, viral – eg enteroviruses such as rotavirus, Tuberculosis
- protozoal – eg giardiasis, amoebiasis).
atypical infective agents can affect the bowel and cause diarrhoea but are more usual in immunosuppressed people (eg renal transplant recipients, HIV/AIDS)
- Pseudomembranous colitis (usually post-antibiotic therapy and characterised by C.difficile toxin secretion)

  1. Coeliac disease (gluten induced enteropathy): often designated an autoimmune disease but is reversible if gluten is avoided
  2. IBD: Crohn’s disease, ulcerative colitis (together called ‘chronic idiopathic inflammatory bowel disease, CIBD or IBD)
79
Q

Main causes of diarrhoea: Vascular disease

A

Vascular disease:
vasculitis, ischaemic enteritis/colitis, radiation enteritis/colitis
(damages small blood vessels)

80
Q

Main causes of diarrhoea: Neoplasia

A

Neoplasia:

  • lymphoma (particularly small bowel) may cause malabsorption,
  • overflow diarrhoea (may complicate carcinoma of distal colon),
  • neuroendocrine tumour (old term ‘carcinoid’ secretes peptides eg 5-HT, which may cause episodic palpitations, flushing and diarrhoea)
81
Q

Gross and microscopical features distinguishing between UC and Crohn’s (revision slide)

A
82
Q

Pattern difference between Crohns and UC

A

Crohns:

  1. transdural inflammation (goes through mucosa, submucosa and muscle, fistula formations w other organs)
  2. skip lesions - patchy

UC:

  1. pseudopolyp
  2. superficial ulceration (active disease) or atrophy (inactive disease)
83
Q 
Proctitis
Proctosigmoiditis
Distal colitis
Pancolitis
Backwash ileutis
A 
Proctitis- only rectum
Proctosigmoiditis- rectum and sigmoid colon
Distal colitis- only left side of colon
Pancolitis- entire colon
Backwash ileitis- distal ileum
84
Q

Clinical features of UC and Crohns revision slide

A
85
Q

Which one is normal and which one is UC?

A
86
Q

What is cobblestone appearance?

A

Irregular nodular appearance of mucosal surface with hyperaemia and focal superficial ulceration

In Crohn’s (small bowel)

87
Q

Faecal calprotectin

A

Calprotectin is a stool (faecal) test that is used to detect inflammation in the intestines. Intestinal inflammation is associated with, for example, some bacterial infections and, in people with inflammatory bowel disease (IBD), it is associated with disease activity and severity.

88
Q

Endoscopy differences between UC and Crohns

A

Crphns:
rectal sparing
cobblestoning
skip areas

UC:
rectum always involved
granularities
inflamed mucosa

89
Q

In what disease is ileal involvement common?

A

Ulcerative colitis

90
Q

In what disease are gripped abscesses more common?

A

Ulcerative colitis

91
Q

Anatomical involvement in Crohns vs UC

A
92
Q

Crohns vs UC macroscopic

A
93
Q

Crohns vs UC macroscopic

A
94
Q

UC vs Crohns disease histology

A
95
Q

What genes is UC more common in?

A

DR2-related genes

95
Q

What genes is UC more common in?

A

DR2-related genes

96
Q

What genes is Crohn’s more common in?

A

DR5 DQ1 alleles

97
Q

Colonic complications in ulcerative colitis

A

Perforation
Bleeding
Cancer
Stricture

98
Q

Crohn’s disease intestinal complications

A 
Perforation
Cancer
Fistula
Abscess
Stricture
99
Q

Other forms of IBD

A

Collagenous colitis/lymphocytic colitis
Ischaemic colitis
Infective colitis
Intermediate colitis - never to be useddd

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