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M104 T1 > M104 T1 L12 > Flashcards

M104 T1 L12 Flashcards

1
Q

What is celiac disease otherwise known as?

A

celiac sprue

gluten-sensitive enteropathy

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2
Q

What main three substances is gluten commonly found in?

A

wheat, rye, and barley

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3
Q

What two substances does gluten consist of?

A

gliadin and glutenins

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4
Q

What genes are associated with Coeliac Disease?

A

HLA - DQ2 gene (95%)

HLA - DQ8 gene (5%)

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5
Q

Which chromosome are the HLA – DQ2 & - DQ8 genes located?

A

CMS 6p21

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6
Q

Is Coeliac disease hereditary?

A

yes - it has a strong hereditary predisposition

affects 10% of first degree relatives

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7
Q

Globally, where is Coeliac disease most prevalent?

A

Western Europe

the USA, especially for those of Irish / Scandinavian descent

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8
Q

Globally, where is Coeliac disease increasing in prevalence?

A

Africa and Asia

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9
Q

Is Coeliac disease a well diagnosed condition?

A

no - a lot of patients in the community are undiagnosed

it requires a high index of suspicion

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10
Q

What conditions have a high prevalence of coeliac disease?

A

Down’s syndrome
Type I diabetes mellitus
auto-immune hepatitis
thyroid gland abnormalities

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11
Q

What percentage of patients with coeliac disease are older than 60?

A

approx 20%

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12
Q

How does gluten cause coeliac disease?

A

Gluten (from diet) + small bowel mucosa produces tissue transglutaminase
this diamidates glutamine in gliadin, producing a negatively charged protein, IL – 15
NK cells + Intraepithelial T lymphocytes results in tissue destruction and villous atrophy

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13
Q

What is transglutaminase otherwise known as?

A

meat glue

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14
Q

What is the role of IL – 15?

A

it stimulates CD8 T cell and NK cells

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15
Q

What types of coeliac disease are there symptoms wise? (ACA)

A

Asymptomatic (detected by a blood test)
Classical coeliac disease
Atypical coeliac disease

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16
Q

What are the symptoms of coeliac disease caused by?

A

the flat mucosa not absorbing nutrients

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17
Q

What are the symptoms of Classical Coeliac Disease?

A 
Diarrhoea
Flatulence (28%)
Borborygmus
Weight loss (45%) 
Weakness & fatigue (80%)
Severe abdominal pain 
IBS-like symptoms
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18
Q

What are the symptoms of Atypical Coeliac Disease?

A

Anaemia (15%)
Osteopenia and osteoporosis
Muscle weakness, pins and needles, loss of balance (minority)
Itchy skin conditions (minority)
Lack of periods (delayed in teens)
infertility and impotence
Bleeding disorders (due to Vitamin K deficiency)

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19
Q

What is an example of an Itchy skin condition?

A

dermatitis herpetiformis

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20
Q

What are the features of an atypical presentation of coeliac disease?

A

Emaciation
Pot belly due to gaseous distention
Muscle wasting
Osteoporosis

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21
Q

What are the general investigations for coeliac disease?

A

FBC, U&Es, LFTs

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22
Q

What are the serological investigations for coeliac disease?

A

the presence of TTGA
the presence of Endomysial IgA
Deamidated gliadin peptide IgA & IgG (new)
For monitoring compliance to gluten free diet
Sero-negative coeliac disease
HLA DQ2 & HLA DQ8 in children with positive TTGA and symptoms to avoid biopsies
Duodenal biopsies

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23
Q

How do routine coeliac disease tests work?

A

They assess tissue damage
When the small bowel is exposed to gluten there is overreaction of the immune system to produce antibodies to the proteins involved in tissue damage

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24
Q

What proteins involved in tissue damage have antibodies produced for them?

A

Tissue transglutaminase
Endomysium
Deamidated gliadin peptide

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25
Q

Where and how many biopsies should be sampled from the intestines?

A

At least four from the duodenum at upper GIT endoscopy as changes can be patchy

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26
Q

What are the microscopic features of Coeliac disease?

A

Villous atrophy
Crypt hyperplasia
Increase in lymphocytes in the lamina propria / chronic inflammation
Increase in intraepithelial lymphocytes
Recovery of villous atrophy on gluten-free diet

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27
Q

What are the complications of coeliac disease?

A

Enteropathy associated T-cell lymphoma
High risk of adenocarcinoma of small bowel and other organs
May be associated with dermatitis hepetiformis
Infertility and miscarriage
Refractory coeliac disease despite strict adherence to gluten free diet

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28
Q

In what organs is there a high risk of adenocarcinomas developing as a complication of coeliac disease?

A

the SI
the large bowel
the oesophagus
the pancreas

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29
Q

What may reduce risk of complications for coeliac disease?

A

a gluten free diet

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30
Q

What conditions come under IBD?

A 
CD, UC
Diverticular disease
Ischaemic colitis
Drug-induced colitis – NSAIDs
Infective colitis
idiopathic inflammatory disease
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31
Q

Why is it important to distinguish CD from UC?

A

they have different complications and different surgical procedures

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32
Q

What is Crohn’s disease complicated by?

A

fibrosis and obstructive symptoms

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33
Q

What parts of the GI tract can Crohn’s disease affect?

A

any part of the GIT from mouth to anus

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34
Q

What is the global spread of Crohn’s disease?

A

has a high prevalence in the Western world
has an increasing incidence in Africa, South America and Asia
Bimodal presentation with peaks in the teens-20s and 60-70 year olds

35
Q

What group is Crohn’s disease especially high in?

A

in patients of Jewish origin

36
Q

What is the cause of CD?

A

exact cause is unknown
there are – all have been implicated
Defects in mucosal barriers allow pathogens and other antigens to induce an unregulated inflammatory reaction

37
Q

What are the factors that potentially contribute to CD?

A

genetic, infectious, dietary, immunologic, smoking, environmental, vascular (GIDISEV)
NSAIDs and psychological factors

38
Q

What are the genetics of CD?

A

genetic predisposition is highly probable

No classical Mendelian inheritance but polygenic

39
Q

What are the genes that could lead to a genetic predisposition towards CD?

A

NOD2 gene

CARD15 gene on cms 16

40
Q

What does the CARD15 on cms 16 code for?

A

a protein associated with uncontrolled inflammatory response to luminal contents and microbes

41
Q

What is the increased risk first degree relatives have of developing CD?

A

13-18% increased risk of with a 50% concordance in monozygotic twins

42
Q

Is there a possible infectious cause of CD?

A

bc granulomas are present in 60-65% of patients, mycobacterium para-tuberculosis was extensively investigated as a possible cause but never proven

43
Q

What infectious organisms have been implicated as possible infectious causes of CD?

A

mycobacterium para-tuberculosis
measles virus
pseudomonas
listeria

44
Q

What are the dangerous effects of listeriosis?

A

fever, meningitis

miscarriage, premature birth

45
Q

How is listeriosis spread?

A

by eating food contaminated with listeria

46
Q

What groups of people does listeriosis primarily affect?

A

pregnant women, newborns

the elderly, people with weakened immune systems

47
Q

What environmental factors are implicated in Crohn’s Disease?

A

Improved Hygiene Hypothesis
Migration from a low risk population to high risk population increases the risk of developing CD
Cigarette smoking doubles the risk of developing CD

48
Q

What does the Improved Hygiene Hypothesis state?

A

that improved hygiene in susceptible individuals reduces enteric infections
this reduces the ability of the GIT mucosa to develop regulatory processes that would normally limit immune response to pathogens which cause self-limiting infections

49
Q

What are the clinical features of CD?

A

Chronic, indolent course punctuated by periods of remission and relapses
Abdominal pain, relieved by opening bowels
Prolonged non-bloody diarrhoea
Blood may be present if the colon is involved
Loss of weight, low grade fever

50
Q

What is the distribution of CD?

A

Small bowel alone – 40%
Large bowel alone – 30%
Small and large bowel – 30%

51
Q

What are the morphological features of CD?

A

Fat wrapping of the serosa
skip lesions
cobblestone pattern (caused by mucosal ulceration)
strictures (fibrosis)

52
Q

What does fat wrapping of the serosa involve?

A

fat deposition on the anterior surface which is usually fat-free

53
Q

What is the effect of fat wrapping in Crohn’s disease at the time of a surgery

A

it can assist the surgeon to demarcate the extent of the disease in the small bowel

54
Q

What are the microscopic appearances of CD?

A

Transmural / full thickness inflammation of the bowel wall
Mixed acute and chronic inflammation i.e. polymorphs and lymphocytes
Preserved crypt architecture
Mucosal ulceration
Fissuring ulcers (deep crevices)
Granulomas (collection of macrophages) present in 60 - 65%
Fibrosis of the wall

55
Q

What are the complications of CD?

A

Intra-abdominal abscesses
Deep ulcers lead to fistula = communication between two mucosal surfaces
Sinus tract = blind ended tract ends in a “cul de sac”
Obstruction due to adhesions
Obstruction due strictures caused by increased fibrosis
Perianal fistula and sinuses
Risk of adenocarcinoma, but not as high as in UC

56
Q

What is the difference between UC and CD?

A

unlike CD, UC’s inflammatory process is confined to the mucosa and sub-mucosa except in severe cases

57
Q

What is the epidemiology of UC?

A

More common in Western countries with higher prevalence in patients of Jewish descent
Less frequent in Africa, Asia and South America
Can arise at any age but rare before the age of 10
Peaks between 20-25 years with a smaller peak in 55-65 year olds

58
Q

What causes UC?

A

unknown but multiple factors are implicated
Genetic predisposition not as well defined as in CD
High incidence in first degree relatives and high concordance in twins
no specific infective agent has been identified

59
Q

What gene is commonly identified in most patients with UC?

A

HLA-B27 identified in most patients with UC, but not thought to be an aetiological factor

60
Q

How do environmental factors affect UC?

A

Smoking is protective in UC -; cessation of smoking may trigger UC or activate disease in remission
NSAIDs exacerbates UC
Antioxidants Vitamins A & E are found in low levels in UC

61
Q

What are the clinical features of UC?

A 
Intermittent attacks of bloody diarrhoea 
Mucoid diarrhoea
Abdominal pain
Low grade fever
Loss of weight
62
Q

What areas are affected by UC?

A

the large bowel from rectum to the caecum
the rectum only - proctitis
left sided bowel only - splenic flexure to rectum
whole large bowel - total colitis

63
Q

What are the macroscopic features of UC?

A

there are no ulcers on endoscopic examination in early disease, despite the term ‘ulcerative’
there is diffuse mucosal involvement which appears haemorrhagic
with chronicity, the mucosa becomes flat with shortening of the bowel

64
Q

What are the microscopic features of UC?

A

Inflammation confined to the mucosa
Diffuse mixed acute & chronic inflammation
Crypt architecture distortion
In quiescent (inactive) UC, the mucosa may be atrophic with little or few inflammatory cells in the lamina propria

65
Q

What are the complications of UC?

A

Toxic megacolon
Refractory bleeding
Dysplasia / adenocarcinoma in patients at risk

66
Q

What are symptoms of a toxic megacolon?

A

Patient very ill
Bloody diarrhoea
Abdominal distention
Electrolyte imbalance with hypoproteinaemia

67
Q

What patients are at risk of dysplasia or adenocarcinoma complications of UC?

A

patients who have had UC at an early age

patients with total unremitting UC

68
Q

After how many years will a UC patient require annual screening colonoscopy?

A

after 8-10 years

69
Q

What are the extra-intestinal manifestations of CD & UC? (OCAH)

A

Ocular
Cutaneous
Arthropathies
Hepatic

70
Q

What are examples of ocular manifestations of CD & UC?

A

uveitis, iritis, episcleritis

71
Q

What are examples of cutaneous manifestations of CD & UC?

A

erythema nodosum

pyoderma gangrenosum

72
Q

What is an example of arthropathies manifestations of CD & UC?

A

ankylosing spondylitis

73
Q

What is an example of hepatic manifestations of CD & UC?

A

screlosing cholangitis

74
Q

What are the investigations in CD & UC?

A 
FBC, U & Es, LFTs
Inflammatory markers – CRP
Faecal Calprotectin
Endoscopy, biopsies
Radiological imaging
75
Q

What inflammatory marker is tested for when investigating CD & UC?

A

C reactive protein

76
Q

What radiological imaging methods are used to investigate CD & UC?

A

Barium studies

MRI, USS, CT Scan

77
Q

What are the differences in presentation between CD & UC?

A

Bleeding: CD - occasional, UC - very common
Obstruction: CD - common, UC - uncommon
Fistula: CD - common, UC - none
Weight loss: CD - common, UC - uncommon
Perianal disease: CD - common, UC - rare
Distribution: CD - entire GIT, skip lesions / UC - large bowel only, continuous

78
Q

What are the differences in pathology between CD & UC?

A

CD - full thickness, UC - mucosa only
CD - fissuring ulcers, UC - no ulcers early stages
CD - granulomas 60 -65%, UC - no granulomas
CD - crypt architecture preserved, UC - crypt architecture distortion

79
Q

What are the differences in radiology between CD & UC?

A

CD - skip lesions, fistula abscess, fibrotic strictures UC - continuous process

80
Q

What are the differences in cancer risk between CD & UC?

A

CD - increased

UC - much higher 1% at 10yrs of diagnosis

81
Q

What are the differences in the effect of smoking between CD & UC?

A

CD - makes it worse

UC - makes it better

82
Q

Why is a pouch created after surgery in UC patients?

A

as a stool reservoir following the surgical removal of the large bowel

83
Q

What is a pouch created from for UC patients?

A

from the small bowel

84
Q

What is a pouch not created for CD patients?

A

bc of the risk of recurrence

M104 T1 (15 decks)

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