Case 12- SAP Flashcards
What is included in IBD (inflammatory bowel disease)
Ulcerative Colitis (UC) and Crohn’s disease
Inflammatory bowel disease
A chronic inflammatory disorder of the intestinal tract with a remitting and relapsing course
Summary of differences- Crohn’s
1) Involves any part of the GI
2) Disease is patchy- skip lesions
3) Strictures are common
4) Cobblestone appearance
5) Can lead to fistula
6) Unusual to get Toxic megacolon
7) Ulcers are fissuring
8) Transmural lymphocytes
9) Marked fibrosis which leads to strictures
10) Granulomas (round collection of Macrophages)
11) Malignancy potential is low
Summary of differences- UC
1) Colon only
2) Diffuse and continuous
3) From the anus upwards
4) Strictures are rare
5) No fistula
6) More likely to get toxic megacolon
7) Pseudopolyps- normal mucosa that looks like mushrooms
8) The ulceration is undermining- not that deep
9) Mild fibrosis
10) No granulomas
11) High malignancy potential
UC (Ulcerative colitis
A diffuse chronic condition which repeated episodes of inflammation in the rectum and colon cause ulcers and irritation
Pancolitis
Entire colon affected
Distal colitis
Only descending colon and rectum affected
Proctitis
Only rectum affected
Causes of IBD
Genetic factors- family history, more important in Crohn’s than UC
• Protective lifestyle factors- breastfeeding, smoking (in UC)
• Lifestyle risk factors- adverse life events, stress, deression
Smoking (in Crohns)
GI infection
Excessive sanitation
Crohn’s disease
A discontinuous inflammatory condition that affects any part of the GI tract, but mainly affects the ileum, colon and perianal region. There will be skip lesions i.e. part of the bowel which is healthy in-between parts with inflammation
Pathology of IBD
- Decreased gut bacterial diversity
- Inappropriate response of mucosal immune system to flora and luminal antigens
- Triggers an inflammatory response
Examination findings of someone with IBD
End of bed = weight loss, pain, fever, anaemia Finger clubbing Vitamin deficiencies Ulcers Bloating PR examination could see blood/soreness
Lab diagnostics for IBD
FBC = Increased WCC
Hb = Low due to anaemia of chronic disease
CRP = high
Faecal calprotectin = high, neutrophil migration to intestinal mucosa
Main regions which Crohn’s affects
The ileum, colon and perianal regions
History of someone presenting with IBD
Diarrhoea, often bloody (>6 weeks) Abdominal pain Fever Perianal lesions Weight loss Failure to thrive Arthritis Epsicleritis Clubbing
Microscopic pathology changes in Crohn’s disease
Lymphoid aggregates i.e. lymphocyte patches proceeding all the way through the tissues as it is transmural
Fibrosis
Transmural inflammation- inflammation extends through all layers of the bowel wall
Granulomas i.e. large groups of macrophages
Fissuring ulcers - resulting in the loss of the mucosa - resulting in granulation tissue instead - leading to blood due to haemorrhaging
Microscopic pathology changes in UC
Pseudopolyps
Gland destruction - forming crypt abscesses i.e. collection of neutrophils on the gland
Crypts can get worse and become fibrous tissue
Vascular congestion
Loss of mucosal folds
Macroscopic changes in Crohn’s disease
Cobblestoning i.e. ulcers separated by normal mucosa
Ulcers in the mouth
Skip lesions as the pathology is discontinuous
The affected areas - commonly the ileum, colon and anus - will be red and inflamed
Complications of Crohn’s disease
Strictures- wall of the affected area thickens due to fibrosis
Fistulas- abnormal connections between 2 organs, because the bowel is inflamed it presses on and breaks down nearby structures i.e. rectum connects to skin. Increases infection risk
Malabsorption- fistulas can cause protein loss. B12 deficiencies. Problems with bile salts, less fat absorption
Perforation- infection is transmural so bowel contents can enter the sterile abdominal cavity
Macroscopic changes in UC
General continuous inflammation of the affected areas - red and friable
No cobblestones as ulceration is everywhere
Pseudopolyps i.e. mucosa trying to regenerate
Undermining ulceration
Colon may be shortened with a wall of normal thickness
Complications of UC
Toxic megacolon- dilation of large bowel, colon becomes paralysed and is unable to move air/faecal matter. High risk of perforation
Dysplasia- precursor to cancer, abnormal development of cells
Cancer- doubles the risk of colonic carcinoma
Differential diagnosis for IBD
- Infectious gastroenteritis- history tends to be more acute, present with diarrhoea and abdominal pain
- IBS- diagnosed through exclusion. Presents with constipation and diarrhoea, Mucus PR is common. This history is chronic (>6 weeks). The abdominal pain is made better by defecation and worse with stress and other triggers.
- Appendicitis- acute onset abdominal pain. Anorexia, fever and tachycardia. Often adolescents and young age
- Coeliac disease- presents with diarrhea, weight loss, anorexia and failure to thrive.
NICE first line treatment for IBS
Laxatives for constipation - not lactulose (worsens cramps)
Loperamide for diarrhoea
Antispasmodic agents
Treat alongside dietary and lifestyle changes not just pharmacological
Antispasmodic drugs
E.g. atropine sulfare, hyoscine butylbromide or peppermint
Competitive blockers of muscarinic receptors
Therefore blocking the effect of acetlycholine on the enteric plexus
Directly causing relaxation of smooth muscle wall
Decreases the intensity of cramps and contractions
Side effects- dry mouth, blurred vision and cardiac arrhythmias
NICE guidelines second line treatment for IBS
Increase laxative intensity. If severe constipation is lasting >1y give linaclotide but only after you have tried other laxatives
Can give TCAs / SSRIs These block brain-gut pain signals Can help regulate normal bowel movement Only very low dose Only if no response to other drugs
NICE guidelines for third line IBS
Eluxadoline
Only for specialist use
It is a opioid agonist which normalises GI motility
NICE guidelines for UC
Use aminosalicylate acids (5-ASA) i.e. Sulfasalazine
Use topically or combine topical and oral
Oral on its own is much less effective
Use oral prednisolone or topical corticosteroids for contraindications
Stage 2:
Add oral prednisolone as well as the topical 5-ASA
Can add a biological agent e.g. infliximab or adalimumab
These are monoclonal antibodies which target TNF
NICE guidelines for CD
Glucocorticosteroid e.g. prednisolone, methylprednisolone
Or 5-ASA treatment if not severe
If 2 or more flare ups occur in a year:
Immunosuppressant drugs e.g. azathioprine or mercaptopurine, use Methotrexate if patients cant tolerate these drugs
Could also try biological agents e.g. infliximab (TNF monoclonal antibodies)
Aminosalicylate (5-ASA)
E.g. sulfasalazine, mesalazine
Help maintain or induce remission in UC and CD
More effective in UC
Oral or topically rectal administration
If oral we need a pH sensitive coating so they dont get digested before they reach the large intestine
Side effects- cough, Megaloblastic anaemia and Proteinuria
Sulfasalazine
Active component is 5-ASA
This is the only component not absorbed but utilised
Reduces inflammation by removing free radicals
Removes excess prostaglandins and leukocytes
Decreases neutrophil chemotaxis
Side effects include diarrhoea and interstitial nephritis
Glucocorticoids
E.g. prednisolone
Potent anti-inflammatory agents
Help induce remission in CD / UC
Administered orally or by enema/suppository
Not used for long term treatment because of side effects
Stimulate synthesis of anti-inflammatory proteins
Purgative drugs
Increase GI tract motility
Therefore accelerating food passage
Examples are laxatives
Antidiarrheal drugs
Decrease GI tract motility
Loperamide mechanism of action
Antimotility agent, helping decrease diarrhoea
It is an opioid-receptor agonist on u-opioid receptors
Decreases activity of the myenteric plexus
Decreasing smooth muscle tone on the intestinal wall
Therefore decreasing motility
Allows time for more water to be absorbed from the bowel contents
Side effects of Loperamide
Dizziness, headache, nausea, flatulence and constipation
Racedotril
Antidiarrhoeal drug acting as a enkephalinase inhibitor
Prevents the breakdown of opioids
Therefore opioid levels increase in the myenteric plexus
Has an anti-secretory effect i.e. prevents secretion of fluid and electrolytes in to the intestine
Doesn’t modify GI transit time
Methylcellulose mechanism of action
Laxative drug Cant be digested so remains in the GI tract Attracts lots of water in to the colon Producing a softer and bulkier stool This stimulates peristalsis Be careful of dehydration however
Stimulant laxative drugs
E.g. bisacodyl, senna
Stimulate enteric nerves to increase peristalsis
Increases electrolyte and water secretion by intestinal mucosa
Helping with constipation
Linalclotide
It works as a monoclonal antibody against tumour necrosis factors. The drug at therapeutic levels should be limited to the GIT lumen and not be absorbed, so wont be detected in the systemic circulation.
Why is consent important
Upholds autonomy (self-determination_
Different forms of consent
- Implied consent- suggestive conduct i.e. holding out your arm for an injection. Problem different actions can be interpreted differently by different people
- Verbal consent
- Written consent- ensures patient has considered everything, important legally. Used in surgery
3 legal requirements for consent
- Has capacity.
- Has adequate understanding.
- Gives consent without being coerced (voluntary).
Bolam test
Where a body of responsible medical professionals decide whether they think you did the right thing. For example, did you provide enough information about risk factors
The Montgmonery test
States that if a reasonable person would attach significance to the risk the doctor should make the patient aware of it.
Gillick competence
Children under 16 are allowed to give consent if they are Gillick competent, meaning they have sufficient understanding and understand the risks involved
Criteria for using children in research
- You cant gain the information through using adults.
- It is approved by an ethics committee.
- The participant has given consent or consent has been given from the parents, a doctor may consent in emergency situations. The child should not seem to object to the parents consent.
Doctor autonomy
If a patient asks for a procedure that you do not think will be beneficial you can refuse the treatment. However, you must respect a patients decision to refuse treatment even if you disagree.
When would you be able to bypass parent consent
You can still go ahead by referring to the Children act of 1989 which states that child welfare is paramount. But you would need to go to court and get permission. In an emergency situation you can provide the life saving treatment but you must be prepared to defend it in court.
