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Gastrointestinal Physiology and Pathophysiology ☆ > Coeliac disease, IBD (Crohn's disease & UC) > Flashcards

Coeliac disease, IBD (Crohn's disease & UC) Flashcards

1
Q

What is coeliac disease (3)

A
  1. Autoimmune reaction to eating gluten (wheat, barley, rye).
  2. The small intestine becomes inflamed and unable to absorb nutrients
  3. NOT a food allergy
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2
Q

What are the symptoms of coeliac disease (9)

A
  1. Diarrhoea
  2. abdominal pain and bloating
  3. fatigue
  4. malnutrition
  5. weight loss
  6. itchy rash
  7. infertility
  8. nerve damage
  9. disorders that affect co-ordination
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3
Q

What are the risk factors of coeliac disease (4)

A
  1. Affects 1 in 100 people in the UK
  2. Female > male
  3. babies and middle-aged adults
  4. those with T1DM or thyroid disease
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4
Q

How is coeliac disease diagnosed (3)

A
  1. 1st do a blood test to check for antibodies – IgA tissue transglutaminase (tTG)
  2. if comes back positive need to do a biopsy of the intestine lining to confirm the diagnosis
  3. Differential diagnosis: IBS or food allergy?
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5
Q

What treatment is there for coeliac disease

A

Gluten-free diet

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6
Q

What are the complications of coeliac disease (5)

A
  1. Vitamin B12 deficiency
  2. osteoporosis
  3. iron deficiency
  4. infertility
  5. bowel cancer
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7
Q

What public education is there for coeliac disease (11)

A
  1. Promote an awareness of the condition, prompting earlier diagnosis
  2. Highlight the availability of gluten-free foods in supermarkets, push away from prescribing (cost implications)
  3. Promote adherence to avoiding gluten-free foods, educate on risks of not doing
  4. Be aware of red-flag symptoms and promptly refer the patient to the doctor
  5. Recommendation of calcium/ vitamin D supplements
  6. Educate on symptoms of iron deficiency
  7. Flu vaccine
  8. smoking cessation
  9. physical exercise
  10. limitations on alcohol consumption
  11. Ensure the patient is followed up at least annually
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8
Q

what are the red flag symptoms of coeliac disease (3)

A
  1. Blood in stools
  2. Poor response/ weight loss on gluten-free diet
  3. Unexplained abdominal pain
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9
Q

What is IBD: ulcerative colitis and Crohn’s disease (4)

A
  1. A broad term to describe chronic non-specific inflammatory conditions of the gastro-intestinal tract
  2. IBD = inflammatory bowl disease
  3. Both UC and Crohn’s disease is characterised by unpredictable periods of remission and relapse
  4. Current available medical treatment is not curative
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10
Q

How does age affect IBD: ulcerative colitis and Crohn’s disease (4)

A
  1. Peak 10-40 years
  2. 15% diagnosed at over 60 yrs
  3. 20-30% diagnosed at under 20yrs
  4. No difference between the sexes
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11
Q

How does IBD come about (7)

A
  1. The immune system mistakes “friendly bacteria” in the colon – which aid digestion – as a harmful infection, leading to the colon and rectum becoming inflamed
  2. Bringing about a severe, prolonged, inappropriate inflammatory response
  3. Increased activity of effector lymphocytes & pro-inflammatory cytokines
  4. Primary failure of regulatory lymphocytes & cytokines e.g.IL-10
  5. T cell resistance to apoptosis after inactivation (CD)
  6. Non-pathogenic bowel flora appear to be an essential factor
  7. Alteration in normal architecture of GI tract, leading to symptoms of IBD (e.g. alteration of the multiple levels of infolding of the four-layered mucosal walls)
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12
Q

What are the differences between Ulcerative colitis and Crohn’s disease (4)

A
  1. UC affects the entire large intestine (colon)
  2. CD can affect any part of the digestive tract from the mouth to anus
  3. UC = Haustra- small pouches of the colon which give the colon its segmented appearance.
  4. CD = thickening, strictures & ulcers.
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13
Q

what factors cause IBD (5)

A
  1. Genetic
  2. Protein diet
  3. Smoking
  4. Certain infections
  5. Altered gut microflora
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14
Q

How does genes cause IBD

A

15% first degree relatives

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15
Q

How do protein diets cause IBD

A

High animal protein diet (Increased Hydrogen Sulphide)

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16
Q

How does smoking cause IBD (7)

A
  1. CD, 2x more common in smokers
  2. UC, 3x more common in ex-smokers or non-smokers (i.e. smoking protects in UC!)
  3. Smoking cause more relapses
  4. Smoking causes more pain
  5. Smoking leads to more operations
  6. Smoking lowers QOL
  7. If you stop smoking for more than 1 year, CD has a much more benign course
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17
Q

How does certain infections cause IBD

A

Mycobacterium paratuberculosis in CD – causative (also implicated in RA)

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18
Q

How does altered gut microflora cause IBD (3)

A
  1. People with IBD have found to have significantly reduced biodiversity of beneficial gut microflora
  2. Beneficial bacteria produce anti-inflammatory products, protective antibodies, and neutralise pathogens
  3. Antibiotics and certain foods change the composition of the gut microflora
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19
Q

How does the Helminth parasite affect IBD (5)

A
  1. Helminths = intestinal (usually) parasitic worms
  2. Common in poor counties & children (poor sanitation/hygiene)
  3. IBD rare where helminth infection common!
  4. Hygiene hypothesis: hygiene practices increases risk of certain immunological disorders
  5. Induction of regulatory T cells and modulatory cytokines
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20
Q

How are helminths transmitted from human to human (6)

A
  1. females lay eggs on perianal folds
  2. Larvae in the eggs mature within four to six hours
  3. embryonated eggs are ingested by a human
  4. larvae hatch in the small intestine
  5. adults in lumrn of cercum
  6. gravid female migrates to perianal region at night to lay eggs
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21
Q

How are helminths transmitted from soil to human (8)

A
  1. fertilised eggs ingested in food or soil
  2. egg becomes larval worm and penetrates wall of duodenum → the venous system from the liver to the heart
  3. eggs enters pulmonary circulation
  4. larvae break alveoli, grow and moult
  5. larvae passes from the respiratory system to be coughed up and swallowed
  6. larve returns to the small intestine where they mature into adults
  7. eggs are passed in faeces
  8. infective larvae develops within fertilised egg in soil where they can persist for ten years or more
22
Q

What are the red flag symptoms of UC (7)

A
  1. Diarrhoea
  2. Abdominal Pain (LL Quad) (lower left)
  3. Rectal bleeding
  4. Mucorrhoea
  5. Abdominal pain
  6. Tenesmus – cramping rectal pain/ urgency
  7. Incontinence
23
Q

What are the red flag symptoms of Crohn’s disease (7)

A
  1. Diarrhoea
  2. Abdominal Pain
  3. Mass (tender)
  4. Abdominal distension
  5. Weight loss
  6. Anaemia
  7. Extra intestinal manifestations…
24
Q

What are the extra-intestinal symptoms of crohn’s disease (19)

A
  1. Uveitis - inflammation of the middle layer of the eye, uvea
  2. Liver disease
  3. Ankylosinf spindylitis
  4. Peripheral arthritis
  5. Finger clubbing
  6. Pyoderma gangrenosum
  7. Erythema nodosum
  8. Growth retardation
  9. decreased zinc: taste impaired
  10. decreased vitamin b12: anaemia
  11. decreased folate: anaemia
  12. decreased iron: anaemia
  13. decreased vitamin k: bruises
  14. decreased potassium: lethargy, ileus
  15. decreased calcium & magnesium: tetany
  16. decreased vitamin c: scurvy
  17. Osteoporosis
  18. Emacipation
  19. Hypoproteniaemia: odeama
25
Q

What are normal bowl movements and what is diarrhoea (2)

A
  1. Normal bowel movements: One every THREE days to one THREE times a day
  2. Diarrhoea: “Loose” movements
26
Q

What is the aim in IBD treatment (5)

A
  1. treat flare ups quickly and maintain remission using pharmacological therapy (and diet)
  2. Therapy not a cure- it is a lifelong prevention of colon cancer
  3. after 10 years the risk of developing bowel cancer is 1 in 50
  4. after 20 years the risk of developing bowel cancer is 1 in 12
  5. after 30 years, the risk of developing bowel cancer is 1 in 6
27
Q

What are the complications to IBD (2)

A
  1. Complications can lead to surgery and stomas (temporary and permanent)
  2. Stoma bags are for diet and digestion
28
Q

How is IBD diagnosed (4)

A
  1. Haematological - FBC, U&Es, inflammatory markers (CRP)
  2. Stool tests – Check not infection e.g. food poisoning/ salmonella/ infective diarrhea and check faecal calprotectin levels
  3. Endoscopic - sigmoidoscopy, colonoscopy, wireless capsule endoscopy (only if non-stricturing CD)
  4. Radiology – AXR, barium enema, CT & MRI, isotope-labelled scans
29
Q

How is UC categorised (6)

A
  1. Disease is categorised in to severe, moderate or mild

Based on:

  1. Bowel movements number
  2. blood in stools
  3. pyrexia (high temperature)
  4. anaemia
  5. erythrocyte sedation
30
Q

What is the CD activity index based on (6)

A
  1. stool frequency
  2. abdominal pain
  3. complications
  4. weight
  5. if taking loperamide or opiates
  6. how ‘well’ the patient is feeling
31
Q

what is the treatment for mild UC and Crohn’s (5)

A
  1. UC = topical aminosalicylate
  2. UC after 4 weeks = oral aminosalicylate then if required + topical/oral corticosteroid
  3. Crohn’s = Oral corticosteroid (prednisolone/methylpred.
  4. Crohn’s = Or budesonide if lower SE needed)
  5. If Corticosteroid contraindicated aminosalicylate
32
Q

what is the treatment for moderate UC and Crohn’s (5)

A
  1. UC = Topical aminosalicylate,
  2. UC after 4 weeks = Topical aminosalicylate + high-dose oral aminosalicylate or switch to a high-dose oral aminosalicylate and time-limited topical corticosteroid
  3. UC = If more needed switch to oral aminosalicylate + oral corticosteroid
  4. Crohn’s = Oral corticosteroid (do not offer budesonide or aminosalicylate as less effective)
  5. If ≥ two exacerbations in 1 year or glucocorticoid dose cannot be tapered, consider (+Azathioprine or mercaptopurine) or +Methotrexate
33
Q

what is the treatment for severe UC and Crohn’s (3)

A
  1. UC = IV corticosteroid (IV ciclosporin as alternative)
  2. UC After 72 hours + IV ciclosporin (+ infliximab if ciclosporin not tolerated)
  3. Crohn’s = If unresponsive to conventional therapy + infliximab or adalimumab
34
Q

How does the location of the issue affect formulation choice (7)

A
  1. Proctitis = topical treatment +/- oral
  2. Left-sided colitis = topical treatment +/- oral
  3. Pancolitis = oral treatment +/- topical
  4. Ascending/transverse colon = orally given: local release of mesalamine
  5. Descending colon = Enemas: reach the splenic flexure
  6. Sigmoid colon = foams
  7. Rectum/15cm beyond anal verge = suppositories
35
Q

Where do 5-aminosalicylates release (9)

A
  1. duodenum/jejunum = pentsa
  2. Ileum = asacol, meszavant, ipocol, salofalk, mesren
  3. Cecum (first part of the large intestine) = Olsalazine, balsalazide, sulfasalazine
36
Q

What is the best treatment for Crohn’s disease (3)

A
  1. Special liquid diets (elemental diets) are the best treatment for CD currently known
  2. e.g. elemental 028 extra
  3. 85-100% of patients will enjoy a full remission IF **they stick to the diet
  4. Can drink or have via NGT (nasogatro tube)
37
Q

How do elemental diets work (5)

A
  1. Elemental diets made from the basic building blocks of foods
  2. normal processes of digestion in the gut not required
  3. Virtually 100% of the nourishment is absorbed into the body high in the small intestine
  4. little if any left to be metabolised by the bacteria which live lower down in the intestine leading to healing.
  5. Food is reintroduced slowly over 2-3 months
38
Q

What is the chronic treatment of Proctitis/ proctosigmoiditis (rectal inflammation) (3)

A
  1. Topical aminosalicylate
  2. Topical + oral aminosalicylate (oral ideally OD)
  3. Oral aminosalicylate alone- explaining not as effective
39
Q

What is the chronic treatment of left sided and extensive UC

A

Oral aminosalicylate (ideally OD)

40
Q

What is the chronic treatment of all extents of UC (3)

A
  1. If oral aminosalicylate not effective, not tolerated or ≥ 2 exacerbations in a year
  2. Oral azathioprine
  3. or mercaptopurine
41
Q

What is the chronic treatment of Crohn’s disease where no medication is being given (2)

A
  1. Agree plans for follow up frequency and who to see
  2. Education on symptoms and not smoking
42
Q

What is the chronic treatment of Crohn’s disease (3)

A
  1. Azathioprine or mercaptopurine monotherapy
  2. Methotrexate where Aza/MCP not tolerated
  3. Do NOT offer corticosteroid
43
Q

When are steroids used (2)

A
  1. Only used in acute management – NOT maintenance therapy
  2. Not effective in maintenance therapy and many issues with long term use
44
Q

what are the adverse effects from high dose or long-term steroid use (7)

A
  1. Cushing’s like features (47%):
  2. Hypertension (13%)
  3. Diabetes (10x relative risk increase)
  4. Osteonecrosis (4%)
  5. Glaucoma (↑ intraocular pressure)
  6. Growth retardation
  7. Skin atrophy
45
Q

what must all patients in high/long dose steroids have (3)

A
  1. Steroid card- do not stop suddenly (adrenal insufficiency)
  2. Bone protection (calcium tablets)
  3. GI protection (PPI)
46
Q

How are aminosalicylates used (3)

A
  1. Contain 5-aminosalicylate. Released at different points in gut
  2. Immunomodulatory, antibacterial and affect the arachidonic acid pathway (= complicated)
  3. More effective in UC
47
Q

what are the side effects of aminosalicylates (5)

A
  1. Diarrhoea
  2. Headache
  3. N & V
  4. abdominal pain
  5. rash
48
Q

What counselling/monitoring is there for aminosalicylates (8)

A
  1. monitor renal function
  2. carry out FBC’s (full blood counts).
  3. patient must report unexplained bruising
  4. patient must report sore throat
  5. patient must report bleeding
  6. patient must report fever
  7. patient must report tiredness
  8. these are signs on blood dyscrasias
49
Q

How are immunosuppressants used (6)

A
  1. Azathioprine Pro-drug → Mercaptopurine (6-MP)
  2. Inhibits purine synthesis needed for DNA/RNA production → reduced white blood cell production → immunosuppression
  3. Metabolised by thiopurine methyltransferase (TPMT)
  4. TPMT activity low → Increased activity → increased bone marrow suppression
  5. Hence TPMT test before treatment
  6. Used in immunosuppression in a variety of conditions (e.g., RA, Lupus, transplant…)
50
Q

How are Anti-TNF drugs used (Anti-Tumour Necrosis Factor) (2)

A
  1. TNF is a pro-inflammatory protein
  2. Therefore blocking it reduces inflammation
51
Q

What are the side effects of anti-TNF drugs (6)

A
  1. Risk serious infections
  2. Muscle aches
  3. GI disturbances
  4. BP disturbances
  5. cholesterol disturbances
  6. sleep disturbances
52
Q

What signs must be reported when on anti-TNF drugs (3)

A
  1. TB - persistent cough, weight loss, fever
  2. Infection - sore throat, bruising, fever
  3. Delayed hypersensitivity - rash, itching, breathing problems, chest pain, fever

Gastrointestinal Physiology and Pathophysiology ☆ (24 decks)

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