IBD Flashcards
what type of bug is TB
acid fast bacilli
what is crohns disease
chronic inflammatory and ulcerating condition of the GI tract that can affect anywhere from the mouth to the anus
where is crohns most common
terminal ileum and colon
what is the most common age group for crohns diagnosis
early 20s (50% 20-20, 90% 10-40)- commoner in males
other than the bowl where can crohns affect
stomach, oesophagus, mouth, rectum/anus
what is the presentation of crohns
abdominal pain (colicky), small bowl obstruction, diarrhoea, bleeding PR, anaemia, weight loss, tender abdomen
is crohns curable
no but patients can go into lasting remission
what investigations should be done for crohns
endoscopy and mucosal biopsy
what appearance is seen in endoscopy
cobble-stone appearance
what is the endoscopic pattern of crohns disease
Patchy, segmental disease with skip areas (lesions) anywhere in GI tract
(skip areas= bits of unharmed tissue surrounded by damaged tissue)
what does the normal colonic mucosa look like
crypts packed together like rack of test tubes
describe a biopsy of crohns
chronic inflammation in lamina propria (fills with inflammatory cells)
- cryptisis
- crypts are irregular shape- look shattered
- crypt abscess can form
- granulomas (macrophages in a tight ball like sarcoidosis) non caseating
- transmural inflammation
- deep knife like fissuring ulcers
describe a non caseating granuloma
abnormal collection of macrophages and derivates such as giant cells that do not show a soft centre
are granulomas always found in crohns
no 50% of people dont
how does crohns cause bowl obstruction
fibrosis- stricture- obstruction
what happens to the wall of the bowl in crohns
is thickened- deep fissuring ulceration destroys mucosa (cobble stoning)
why does anaemia, fatigue, weight loss and diarrhoea happen in crohns
as lumen filled with pus- cannot absorb aswell
what types of polyps might be seen in crohns
pseudopolyps
how is crohns transmural inflammation
affects all 3 layers of the bowel
what are the complications of crohns
malabsorption, fistulas, intractable disease, bowl obstruction, anal disease, perforation, malignancy, amyloidosis, rarely toxic megacolon
what is an iatrogenic cause of malabsorption in crohns
short bowl syndrome due to repeated resections and recurrences
what can result from malabsorption in crohns
Hypoproteinemia, Vitamin deficiency, Anaemia, gallstones
what type of anaemia does iron deficiency lead to
microlytic- small red blood cells
what is macrolytic anaemia and what causes it
blood with an insufficient concentration of hemoglobin- red blood cells larger than normal
vitamin B12 and folate deficiency
what is blind loop syndrome
bacterial overgrowth in the small intestine
what is included in anal disease in crohns
sinuses, fissures, skin tags, abscesses, perineum falls apart
what is intractable disease from crohns
failure to tolerate or respond to medical therapy, continuous diarrhoea or pain, may require surgery, not curative
what is amyloidosis
a rare disease that occurs when a substance called amyloid builds up in your organs
what is amyloid
an abnormal protein that in produced in bone marrow
what is toxic megacolon
dilated bowel
where does crohns and UC have a high incidence
north america and northern europe, high in scotland
what genetic defects are associated with crohns
NOD2 (CARD15)on chromosome 16
(encodes a protein in bacterial recognition)
HLA-DR1
HLA-DQw5
what are the environmental triggers to crohns
smoking increases risk
infectious agents (viral, mycobacterium) cause similar pathology
vascilutis could explain segmental distribution
sterile environment theory
what autoimmune features could cause crohns
persistent T cell and macrophage activation
excess pro inflammatory cytokine production
why do gene defects cause crohns
as they prevent a controlled effective immune response to a trigger (more susceptible to environmental agents)
what is ulcerative colitis
chronic inflammatory (mucosal and submucosal inflammation) disorder confined to the colon and rectum of unknwon aetiology
bloody diarrhoea with infection excluded= think what?
UC
what age group has peak incidence
30s, can occur in any
where does UC affect
confined to colon and rectum
where in GI tract does crohns usually spare
the rectum
what is the clinical presentation of UC
diarrhoea, mucus and blood PR
what are the different onsets of UC
chronic course with exacerbation and remission
continuous low grade activity
a single attack
an acute colitis (toxic megacolon)
what investigations should be done for UC- bloody diarrhoea and mucous
endoscopy and mucosal biopsy
what is seen on an endoscopy in UC
red inflamed rectum- diffusely ulcerated, almost always involving the rectum
what does UC never go higher than
the ileoceacal valve
describe a biopsy of UC
massive influx of inflammatory cell- colonic mucosa gone, no barrier, infiltrate of inflammatory cells in the submucosa destroying the crypts
crypts are irregularly shaped and branching- acute cryptitis
crypt abscesses
severe ulceration with fibrinopurulent exudate
what are the features of chronic inactive UC
low grade chronic inflammation with crypt distortion and low grade diarrhoea
what is a surgery used in severe UC
subtotal colectomy- bowl removed
what can cure UC
removal of the large bowl
are pseudopolyps seen in UC
yes
where in inflammation confined to in UC
the mucosa and submucosa (except in toxic megacolon) SUPERFICIAL ULCERATION
are there granulomas in UC
no
what are the complications of UC
intractable disease, toxic megacolon, colorectal carcinoma, blood loss, electrolyte disturbance, anal fissures, extra GI manifestations: eyes, liver, joints, skin,
describe intractable disease in UC
continuous diarrhoea, flares may be due to intercurrent infection by enteric bacteria or CMV (cytomegalovirus)
describe toxic megacolon
acute or acute on chronic (an exacerbation) fulminant colitis- colon swells and will rupture unless removed by emergency colectomy- colon fills with fluid, pus and blood
why does UC lead to colorectal cancer
as chronic inflammation leads to epithelial dysplasia and then carcinoma
why is more of the colon predisposed to cancer in UC than in crohns
as diffuse not patchy in UC
what electrolyte imbalance in common in UC
hypokalemia
name the extra GI manifestations of UC
eyes- uveitis
liver- primary sclerosing cholangitis (autoimmune destruction of bile ducts)
joints- arthritis, ank spondylitis
skin- pyoderma gangrenosum, erythema nodusum
what gene is UC associated with
HLA-DR2
NOD-2 (familial cases)
(immune system at fault)
what is aberrant immune response
autoimmune disease
describe the autoimmune response in UC
persistent activation of T cells and macrophages
autoantibodies (e.g. ANCA)
excess proinflammatory cytokine production
bystander damage due to neutrophillic inflammation
what might alter the autoimmune response in both UC and crohns
probiotics (as microbiome is abnormal)
what are the environmental trigger of UC
unknown- smoking actually help
in UC or crohns are fistula more common
in crohns- UC superficial ulceration
what has a higher cancer risk UC or crohns
UC
in UC or crohns is extra GI symptoms more common
UC
what is the clinical presentation of crohns
abdominal pain and peri-anal disease
what is the clinical presentation of UC
diarrhoea and bleeding
what are the three components of the pathogenesis of IBD
genetic disposition
mucosal immune system
environmental triggers
what does over reactive effector T cells do
inflammation/ disease
what does an absence of regulatory T cells cause
uncontrolled inflammation/ aggressive disease
what immune factor mediates crohns
Th1 mediates
what immune factor mediates UC
mixed Th1/ Th2 mediated disease/ NKTC
which does smoking aggravate, UC or crohns
crohns
what should you avoid in crohns
NSAIDS e.g. ibruprofen
what are the symptoms of UC
Diarrhoea + bleeding Increased bowel frequency (HOW OFTEN?) Urgency Tenesmus Incontinence Night rising- shouldn’t have to poo at night Lower abdo pain (esp. LIF) (proctitis can cause constipation
what diarrhoea can antibiotics cause
C diff
what is a severe UC episode
>6 bloody stools/24 hour \+ 1 or more of Fever Tachycardia Anaemia Elevated ESR
what further assessments should you do
bloods: CRP, albumin
plain AXR
endoscopy
histology
what is absent in an inflammed colon
stool
what is seen on a AXR in UC
stool distribution- Bowl black as full of acid, lack of stool
Mucosal oedema / ‘thumb-printing’- swelling of the mucosal bowel wall, thickens
toxin megacolon
what can be seen on an endoscopy in UC
Loss of vessel pattern
Granular mucosa
Contact bleeding- inflamed tissue friable to bleed
what leads to abscesses in UC
distortion of crypts
what determines the risk of colorectal cancer
severity of inflammation
duration of disease
disease extent
what is primary sclerosing cholangitis
chronic inflammatory disease of biliary tree- 80% have associated IBD
what is peri-anal disease
recurrent abscess formation- pain, can lead to fistula with persistent leakage, damaged sphincters
what determines the symptoms of crohns
the site of the disease
what are the symptoms of crohns in the small intestine
abdominal cramps, diarrhoea, weight loss
what are the symptoms of crohns in the colon
abdominal cramps
diarrhoea with blood
weight loss
what are the symptoms of crohns in the mouth
painful ulcers,
swollen lips,
angular chielitis
what are the symptoms of crohns in the anus
peri-anal pain,
abscess
what blood abnormalities would suggest crohns
CRP, albumin, platelets, B12 (terminal ileum B12 deficiency), ferritin
loss of haustra markers can lead to what
formation of a fistula= crohns
what small bowel assessments could be done in crohns
Barium follow-through
Small bowel MRI (gold standard with intravenous and swallow contrast)
Technetium-labelled white cell scan
what lifestyle changes can help in IBD
smoking cessation- crohns
diet- low residue (fibre) diet so bowel doesn’t have to work as hard
what does smoking cause recurrence in 70% of cases
crohns relapse
what is the treatment for UC
5ASA (mesalazine)
steroids (acute/ severe flare not long term)
immunosuppressants (steroid sparing agents)
anti-TNF therapy
what is the treatment for crohns
steroids (acute/ severe
flare not long term)
immunosuppressants (maintenance therapy)
anti TNF therapy
what is the mechanisms of action of 5 ASA
acts on mucosal surface, has a topical anti inflammatory effect. reduces the risk of colon cancer
what are the side effects of 5ASA
diarrhoea, idiosyncratic nephritis - monitor renal function before and during
what are the two ways 5 ASA can be administered
oral (tablets or granules)- delayed, pH dependant release
topical= suppositories, enemas
what part of the GI tract do ALL 5-ASA conjugates reach
the colon
what are the pros/ cons of suppositories and enemas
suppositories: only reach 20cm but adhere to mucosa better
enemas: go further but don’t adhere as well
what is the mechanisms of action of corticosteroids in IBD
systemic anti-inflammatory properties, to induce remission
what are the two types of administration of corticosteroids in IBD and examples of each
oral; prednisolone (has more systemic effects)
topical: budesonide (less SE as less first pass metabolism)
short course- high dose initially reducing over 6-8 weeks
why should steroids be used as a bridge to maintenance therapy + what are the side effects
as people become dependant + side effects;
- musculoskeletal (avascular necrosis, osteoperosis)
- GI
- cutaneous (ance, thinning of skin)
- metabolic (weight gain -increased appeptite- diabetes, hypertension)
- neuropsychiatric (trouble sleeping, manic, depressed)
- cataracts
- growth failure in children
give examples of immunosupression therapies in IBD
azathioprine/ mercaptopurine
methotrexate
what is the active for of azathioprine
6-TGN
what should you avoid prescribing azathioprine with
allopurinol
what are the side effects of azathioprine
pancreatitis
leucopaenia
hepatitis
small skin of lymphoma, skin cancer
what immune response is associated with crohns
Th1 cells, production of interleukins and TNF-alpha by DC cells and macrophages
Polarized T cell responses initiate an inflammatory cascade that involves endothelial activation, chemokine production, and white blood cell (WBC) recruitment.
what secretes IL2, 17, IFN-y and TNF-alpha
Th1 polarised cells
what immune response is associated with UC
Th2 and NK cells
Polarized T cell responses initiate an inflammatory cascade that involves endothelial activation, chemokine production, and white blood cell (WBC) recruitment.
what cells are targeted in the immunosupression therapies for IBD
tnf- alpha, MadCAM-1, T cells
what is tumour necrosis factor alpha
a proinflammatory cytokine
what are the antibodies fto TNF
infliximab; IV infusion
adalimumab; S/C injection
how does anti TNF therapy work
promotes apoptosis of activates T-lymphocytes, rapid onset of action
why might anti-TNFa treatments be unsafe
patient may already have antibodies that block the action of the drug
infections could develop
TB and tumours may reactivate
when should Anti-TNFa therapy be used
as part of long term strategy, including immune suppression, surgery (Crohns), supportive therapy
refractory / fistulising disease
name three anti- TNFa therapies
infliximab, remicade, inflectra, remsima
when is emergency therapy done in IBD
where there is failure to respond to medical therapy, small bowel obstruction, abscess, fistulae
when is elective surgery done in IBD
when there is failure to respond to therapy, dysplasia of colon mucosa
for which IBD can surgery be curable
UC- permanent ileostomy/ restorative proctocoloectomy and pouch
what is a proctocolectomy
surgical removal of the rectum and all/part of the colon
what is a proctocolectomy with end ileostomy
where the anus is sewed shut and a stoma inserted into the skin of the lower abdomen
what are the indications for elective surgery in UC
medically unresponsive disease,
intolerability,
dysplasia/ malignancy,
growth retardation in children
what are the different end of an elective proctocolectomy
ileostomy, a pouch, ileorectal anastomosis
what are the pros and cons of a pouch
patient can go to the toilet but average 6 bowel movement a day
can have incontinence, nocturnal incontinence/leakage/spotting or the pouch can fail
what are the local immediate, early and late complications of a pouch
immediate- haemorrhage, enterotomy
early- urinary dysfunction, wound infection, pelvic abscess, anastomotic leak
late- impotence, infertility, pouchitis
what are the systemic immediate, early and late complications of a pouch
immediate- anaphylaxis
early- atelectasis, ileus (lack of movement in intestines), portal vein thrombosis
late- DVT/PE, small bowel obstruction
how do you assess the severity of an acute UC attack
truelove and witt criteria:
ESR (inflammation marker in blood) Haemoglobin Bloody Stools Temperature>37.8 Heart rate>90
what is a subtotal colectomy
resection of part of the colon
what are nervi erigenti
pelvic splanchnic
what are the indications for surgery in crohns
Stenosis causing obstruction Enterocutaneous fistulas Intra-abdominal fistulas Abscesses Bleeding (acute or chronic) Free perforation
when is a gastrojejunostomy done
for duodenal or pyloric stenosis
what can be used instead of resection to treate strictures in crohns
stricturoplasty- balloon dilatation
what is an enterocutaneuos fistula
an abnormal connection between the intestines/ stomach and the skin of the abdominal wall
what are the different types of lesions in perianal disease
primary- fissure, ulcer
secondary- abscess, tags, fistula
incidental- piles hidradenitits
what type of IBD can be cured by surgery
UC
what are the common deficiencies in IBD
anaemia, oestoperosis, B12, folate
what is modulen
nutritional powder
