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Session 5: GI Flashcards

1
Q

What is IBD and what are the two types?

A

A chronic inflammatory bowel disease which follows a protracted relapsing and remitting course. The two types are Ulcerative colitis and Crohns

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2
Q

What is Ulcerative Colitis?

A

Inflammation of the rectal and sigmoid colon (proctitis) Inflammation spreads proximally from the rectal sigmoid to the descending colon.

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3
Q

What are the symptoms of UC?

A
  • Colicky abdominal pain
  • bloody diarrhoea
  • tenesmus
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4
Q

What are the extraintestinal symptoms of UC?

A
  • Iron deficiency anaemia
  • arthritis
  • uveitis
  • skin lesions
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5
Q

What are the complications of UC?

A

Severe GI bleeding
Fulminant colitis
toxic megacolon
perforation with peritonitis
Increased risk for colorectal cancer

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6
Q

Where is UC inflammation present?

A

Superficial inflammation in mucosa and superficial mucosa only

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7
Q

Give an overview of the pathophysiology of UC

A
  1. Destructive immune response initiated by antigens, mediated by lymphocytes of the Th2 phenotype in UC
  2. Increase IL-13 which produces NKT cells reacting to antigens presented in epithelial cells (why it’s more superficial)
  3. genetic association between TNF-a and UC. NKT cells produce TNFa
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8
Q

What are the macroscopic signs of UC?

A

Continuous inflammation, inflammatory polyps and redness

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9
Q

What is Crohn’s mostly caused by?

A

Abnormal Th1 cellular response. Smoking is a risk factor

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10
Q

How does Crohn’s inflammation present?

A

Anywhere in the GI tract and is transmural but the rectum is often spared. Most severe in the terminal ileum

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11
Q

What are the GI symtoms of Crohns?

A

Crampy abdominal pain
Watery diarrhoea
Malabsorption symptoms (malnutrition, steatorrhea B12 deficiency
aphthous ulcers in the mouth

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12
Q

What are the extraintestinal symptoms of Crohn’s?

A

Arthritis, uveitis, skin lesions, higher risk of kidney and gallstones

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13
Q

Why does CD patients have a greater risk of kidney and gallstones?

A

Damage to the terminal ileum decreases the absorption of fats and bile salts in the intestine. Fat binds to calcium preventing calcium from binding to oxalates. Free oxalates lead to calcium oxalate stones.

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14
Q

What are the aims of treatment for Crohns?

A

Induction and maintenance of remission and relief and symptoms.

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15
Q

What are the investigations needed when suspecting UC?

A

Microbiology stool sample, faecal calprotectin, flexible colonoscopy

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16
Q

What is the treatment for UC?

A
  1. Commence IV fluids and empirical IV antibiotics
  2. IV hydrocortisone
  3. VTE prophylaxis -LMWH
  4. Follow step-up treatment
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17
Q

What is the therapeutic ladder for IBD?

A

Severe disease

Biologics
Immunomodulation
Steroids
5-ASA

Mild disease

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18
Q

What are new therapeutic targets for IBD?

A

JAK/STAT signalling inhibitors.

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19
Q

What are the three functions of the digestive system?

A
  1. digestion of food and nutrients
  2. Absorption of nutrients into the bloodstream
  3. Elimination of solid wastes
20
Q

What is GALT?

A

Gut-associated lymphoid tissue. Comprised of tonsils and adenoids, Peyer’s patches, interdigitation lymphocytes, plasma cells and lymphocytes present in the lamina propria and mesenteric lymph nodes

21
Q

Whta is the role of GALT?

A

Manage the immune response to the massive antigen exposure experienced by the gut while maintaining a potent adaptive immune response tonprotect the host from mucosal pathogens

22
Q

What is IBS?

A
  • Common gut-brain Disorder
  • Associated with pain and changes in bowel function.
    Chronic and severe effect, can dramatically affect the Quality of life
  • can be treated effectively.
23
Q

What are the potential factors that determine the manifestation of IBS syndrome?

A

Environment: Acute/ Chronic stressors, life experiences, antibiotics, GI infection, diet
Genes: Regulation pf ut function (motility, sesnory secretion), visceral afferent function, GI immune sytem, Gi micobiome

24
Q

How is IBS diagnosed?

A

Manning’s criteria
Three or more features should have been present for at least 6 months
- pain relief by defecation
- pain onset associated with more frequent stools
- looser stools with pain onset
- abdominal pain onset
-abdominal distention
-mucus in stool
- feeling incomplete poo

25
What are the subtypes of IBS?
Diarrhoea predominant Constipation predominant Pain predominant
26
What is the conservative treatment for diarrhoea-predominant IBS?
Increase dietary fibre
27
Pharmacological treatment for diarrhoea IBS?
-Loperamide (anti-motility drugs) - does not penetrate BBB - MOA: acts on mu-opioid receptors on the neral plexus of the intestines Decreases peristalsis and increases transit time. Increases water absorption and stool firmness.
28
What do we have to be aware of when using Loperamide, especially in patients with IBS?
- can cause drowsiness - could increase the risk of toxic megacolon and perforation
29
What treatment would you use for constipation predominant IBS? And what to avoid?
- increased fibre - bulk laxatives - simulant laxatives may make the symptoms worse
30
What treatment would you use for pain predominant IBS?
-Antispasmodics -Mebeverine (smooth muscle relaxant, first choice) -Hyoscine (buscopan) 10mg can be added -Bloating may be helped by peppermint oil
31
What is the epidemiology of IBD?
-Both sexes equally affected -1st degree relatives 4-20 fold increased risk, up to 7% increased absolute risk -Familial history increases risk of Crohn's more than UC.
32
What is the gut's inflammatory response?
1. leukocytosis - neutrophils enter the blood from the bone marrow 2. margination - neutrophils cling to the capillary wall 3. Diapedisis - neutrophils flatten and squeeze out of the capillaries 4. Chemotaxis - neutrophils follow a chemical trail in response to inflammatory chemcials diffusing from the site of damage as chemotactic agents
33
What are the risk factors for IBD?
Environment: diet, smoking, antibiotics, latitude Microbiome: Increased enterobacteriaeae and fusobacteriaeae. Decreased Clostridales and Bacterodales Immunology: Impaired endothelial function, immunodusregulation, over-reactive response to autophagy Genetics: IBDS, IL23R, AIG16L1, NOD2
34
How does NOD2 act in Crohn's disease?
In healthy gut, RIP2 interacts with NOD2 on Paneth cells in the GIT's mucosal layer to mediate downstream signalling, leading to activation of NF-kappaB which stimulates production of anti-bacterial compounds. In Crohn's disease, mutated NOD2 prevents this cascade and the production of anti-bacterial compounds, leading to dysbacteria and a resultant pro-inflammatory response by Th1 CD4 T cells.
35
How does Crohn's present in endoscopy imaging?
Wall thickening, intramural oedema, inner wall hyperenhancement Wall thickening- only measure bowel loops distended by enteric content. Measure thickest portion or site of most severe inflammation.
36
What is faecal calprotectin used for?
Sensitive marker for inflammation of GI tract, useful for differentiation of IBD vs IBS. Used for diagnosis, monitoring disease activity, treatment guidance and prediction of disease response in post-op IBD.
37
What medications can be used in IBD, give examples.
Glucocorticoid - Prednisolone, Hydrocortisone Anti-inflammatory - Mesalazine Immunosuppressive - Methotrexate, Azathioprine mAb-Adalimumab, Cetolizumab, Etrolizumab, Golibumab, Infliximab, Ustekinamab, Vedolizumab Tyrosine Kinase inhibitors - Tofoacitinib
38
What anti-inflammatory drugs are used for Ulcerative Colitis?
Aminosalicylates (5-ASA) e.g sulphazine - effective to mild to moderate UC. MOA is unknown but anti-inflammatory and immunosuppressive. Patients who cannot tolerate sulfa take Mesazaline. SE = nausea, rashes, blood disorders
39
What is methotrexate?
Immunosuppressive drug. Anti-cancer but at low doses can be used for RA and IBD. Dampens immune system and decreases the activity and production of cells. Cannot be used in pregnancy due to its teratogenic effect. Side effects - bleeding, chest pain, fever, cough and weakness
40
What are glucocorticoids and what are they used for?
e.g. dexamethasone, prednisolone Lipid-based drugs, based on adrenal steroids, synthesised from cholesterol, released as needed under the influence of ACTH. Monotherapy with a time-limited course of corticosteroids may be used for induction of remission if 5-ASAs are not effective or not tolerated.
41
Why should we be aware of Glucocortiocois?
Should not be used long term due to risk of adverse reactions. topical = low toxicity acute use = acceptable toxicity Chronic use = Severe SE and toxicity
42
What is the MOA of glucocorticoids?
Glucocorticoid binds to glucocorticoid receptors via Hsp90 and is taken into the cell. Steroids reduce the expression of the interleukins, adhesion molecules and COX-2 (responsible for the production of prostaglandins that induce inflammation) Reduces expression of proinflammatory genes/ mediators
43
What are the local and systemic effects of chronic steroid use?
Local immunosuppression via inhalers = candida albicans Local effects on vocal cords = dysphonia (hoarseness) Systemic = red and round ace, HTN, cardiac hypertrophy, purple striae, skin ulcers, muscle wasting, osteoporosis, obesity, emotional disturbance women= hirsutism, amenorrhea men = erectile dysfunction
44
What type of drug is azathioprine and what is its MOA?
Immunosuppressive. Prodrug that is quickly converted to 6-MP by glutathione. 6-MP is metabolised in the liver and the gut by one of three enzymes to form 6-TGN which has immunosuppressive proerties
45
What serious drug interaction occurs with Azathoprine/6-MP?
Allopurinol and Febuvostat. Slow elimination of 6-MP by inhibiting xanthine oxidase. SE= bleeding, chest pain, fever, cough, weakness.
46
Which mAbs are used in IBD and what are their targets
Adalimumab (aka HUMIRA) - TNA alpha (anti-tumour necrosis factor, inhibits inflammatory cascade) SE=abdominal pain, chest pain, syncope, blood in urine, diarrhoea, fever. Etrolizumab - Anti B7 subunit of integrins alpha4B7 and alphaEB7 Usterinamab - Anti IL-12 and IL-23 Vedolizumab - Anti alpha 4B7 integrin

Therapeutics (7 decks)

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