PUD 2 Flashcards

1
Q

what is IBD?

A

it is a group of inflammatory conditions that are characterised by chronic inflammation in the GIT

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2
Q

what are the two main forms of IBD?

A

Chron’s disease and ulcerative colitis

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3
Q

what is the difference between CD and UC?

A

clinical, radiology, history and endoscopic features

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4
Q

what does UC involve?

A

involves the colonic mucosal surface

mostly rectum and sometimes colon

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5
Q

how does UC present?

A

presents with bloody diarrhoea

may be associated with abdominal pain/ need to empty bladder but nothing coming out (tenesmus)

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6
Q

what can UC develop into?

A

procitis, left-sided colitis, or pancolitis

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7
Q

where is CD present?

A

small and large bowel- sometimes limited to small bowel

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8
Q

how does CD present?

A

abscesses, fistulas, strictures

some may have blood loss/ diarrhoea

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9
Q

what are the colonoscopy findings of CD and UC?

A

CD- lesions/ cobble stoning/ ulcerations/ strictures

UC-pseudopolypops

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10
Q

which IBD has more of a risk of developing colon cancer?

A

UC

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11
Q

define incidence and prevlance

A
incidence= the number of people that are newly diagnosed with a condition
prevlance= newly diagnosed and people previously diagnosed
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12
Q

which form of IBD does smoking : help prevent disease or may cause it?

A

CD- may prevent

UC- may cause it

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13
Q

what are the environmental factors that may infleucne IBD?

A

diet-inconclusive evidence

smoking- worsens clinical course and inc risk of relaps

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14
Q

how does the interic microflora influence IBD?

A

bowel commensal microflora- induction and maintenance of chronic inflam process

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15
Q

where are the highest conc of bacterial microflora found?

A

terminal ilieum and colon

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16
Q

how does NSAIDS exacerbate IBD?- diofenac

A

direct inhibiton of prostaglandin synthesis

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17
Q

what drugs aggrevate IBD?

A

nsaids
oral contraceptives
antibiotics

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18
Q

what is an appendectomy?

A

protective in UC

possible inc risk in CD

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19
Q

how does stress aggrevate IBD?

A

triggers relaps

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20
Q

what are the clinical manifestations of CD?

A

present with weight loss/ pain or tender mass/ and diarrhoea with no blood

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21
Q

how is diarrhoea caused?

A

mucosal inflamation

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22
Q

how may small bowel obstruction occur?

A

consequence of fibrosis, inflamation and stricture formation

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23
Q

how is a mid disease characterised?

A

apothous or small superficial ulcerations

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24
Q

how is an active CD characterised?

A

focal information and formation of fistula tracts

25
what happens in active diseases?
bowel wall thickens and becomes narrowed and fibrotic leading to recurrent , bowel obstruction
26
what are the typical symptoms of UC?
bloody diarrhoea with mucus abdominal pain with fever weight loss in severe cases
27
what symptoms do patients with proctitis have?
blood or blood stained mucus mixed with stool or streaked onto it
28
what happens when the blood extendeds beyond the rectum?
blood was mixed with stool
29
what happens when the disease is severe?
liquid stool containing bood stool or fetal matter
30
what are IBD patients at risk of?
osteoporosis and anaemia due to malabsorption
31
what are the common deficiencies of IBD?
vit b12, d,k , folic acid, calcium
32
when are deficiencies more common?
in CD/ in active disease
33
when is calcium absorption reduced?
quinsentive and active IBD
34
what are the extratrantestinal complications assoicated with IBD?
joints/ bone/ skin/eyes/ liver
35
what are the common types of arthritis experienced by patients with IBD?
peripheral arthritis axial arthritis ankylosing spondylitis
36
what are the skin complications associated with IBD?
* Peripheralarthritis * Axialarthritis * Ankylosingspondylitis
37
how many IBE patients have a lower bone density?
30-60%
38
what contributes to lower bone density?
prolonged used of cortacosteroids/ vit d/active inflamation
39
what are the eye problems with IBD?
uveitis/keropathy (abnormality of cornea)/ episcleritis(inflam of outer coating of white eye)/ dry eyes (vit a def)
40
what is the main purpose of the inflam response?
localise and eliminate injury that cause injury | protect against further injury
41
how does CD and UC produce an inflam response?
CD- IL-12 and -23 inc helper T cells | UC- IL-13 release cytokine T cells
42
what kind of a disease is IBD?
auto immune disease- it is associated with gut barrier disorders/ dysbyosis
43
what does the mucosal barrier consists of?
epithelial barrier and antimucosal layer
44
what kind of activity is there is IBD?
PPARy activity | mediate aminosalicate activities in IBD
45
How do you diagnose IBD?
blood tests- inflam medicators and renal and hepatic function tests
46
when should diagnostic testing be done?
done periodically when methotrexate, thiopurines and biological agents are used for treatment
47
what is the gold std diagnosis for IBD?
endoscopy
48
what can MRI be used for in diagnosis?
eidence of fissulate and absesses
49
how is the severity of UC measured?
truelove and witts severity index
50
how do you manage mild to moderate UC?
step 1-proctitis and sigmoiditis left sideded or extensive CD step 2- if no improvement add prinosimolone to amino-salicate stop beclametazone
51
how do you manage acute severe UC?
step 1- IV cortosteroids | step 2- add ciclosporin
52
when is surgery indicated in UC?
stool freq more than 8 times a day rise in body temp tachycardia x ray showing colonic diation
53
how do you manage CD?
assess TPMT activity before offering azathioprine cholonic survealance bone mineral density
54
how do you induce remission of CD?
monotherapy- in first presentation of single exacerbation in 12 months enternal nutrition alternative to steroid right-sided- budisamide
55
what do you NOT offer as monotherapy in CD?
Azathioprine, mercaptuprine, or methotrexate as monotherapy
56
what shoud be offered in severe chromes disease?
infleximab, adalimuab
57
when do you offer surgery in CD?
if disease is limited to distal ileum
58
when do you use a stricture in CD?
baloon dialation if single short stricture