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Y2 - BRS - GI > Lower GI Tract > Flashcards

Lower GI Tract Flashcards

1
Q

What does the lower GI tract consist of anatomically?

A

Specifically the large bowel

Cecum (and appendix) –> ascending colon –> transverse colon –> descending colon –> sigmoid colon –> rectum –> anus

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2
Q

What is the blood supply to the ileum and colon?

A

Ileum - supplied by branches of the superior mesenteric artery (SMA)

Colon - supplied by branches of the SMA and inferior mesenteric artery (IMA) covers left side of colon

Venous uptake from bowel is through the superior mesenteric vein (SMV) and inferior mesenteric vein (IMV) that join the portal vein which then join the inferior vena cava (IVC)

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3
Q

What are the 4 layers of the colon, starting from innermost to outermost?

A

Innermost

Mucosa - continuous with the epithelium; contains many glands to produce mucin = important in lubricating bowel = easier to pass stool

Submucosa - between the mucosa and muscularis layer; contains the submucosal plexus = enteric nerve supply (e.g. regulating GI blood flow, epithelial function etc.)

Muscularis - made up of the inner circular and outer longitudinal muscles; contains the myenteric plexus = nerve supply for controlling GI motility

Serosa - like a duvet over the other layers containing the blood vessels and nerves

Outermost

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4
Q

What is the sympathetic and parasympathetic nerve supply to the colon?

A

Parasympathetic:
Vagus = ascending colon and most of transverse colon
Pelvic nerves = more distal colon

Sympathetic:
Lower thoracic and upper lumbar spinal cord
Somatic motor fibres of pedunal nerves = external anal sphincter

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5
Q

What is the enteric NS composed of?

Why is the ENS important (especially in the rectum)?

A

Afferent sensory neurons detect pressure
Myenteric plexus in the muscularis layer

Important because:
Pressure detectors send signals to brain - important for emptying process of rectum (i.e. when to poop)
Important in Hirschsprung’s disease (no enteric intramural ganglia) - causes problems passing stool

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6
Q

x

A

x

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7
Q

What are the 6 types of Lower GI disorders and what are some examples of each?

A
  1. Inflammatory
    • Inflammatory Bowel Disease (IBD)
    • Microscopic colitis
  2. Infective
    • C Diff
    • E Coli .. etc
  3. Structural
    • Diverticular disease
    • Haemorrhoids
    • Fissures
  4. Functional
    • Irritable bowel syndrome
  5. Neoplastic
    • Colonic polyps & colon cancer
  6. Other
    • Neurological, metabolic & vascular
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8
Q

What is inflammatory bowel disease (IBD)?

A

Comprised of Crohn’s disease and Ulcerative colitis

Lifelong chronic disease characterised by inflammation in the bowel, often affecting young people

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9
Q

What is the peidemiology of IBD?

A

Affects 1.5 million people in America and 2.2 million in Europe

New Zealand and Australia have particularly high rates of IBD

Several hundred thousand more worldwide

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10
Q

Why is IBD increasing worldwide?

A

Increasing number of IBD worldwide

Mixing of genetic pool, migration and movement of people

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11
Q

What is the health burden of IBD?

A

Due to chronicness of disease, patients require lifelong treatment

This is a huge health burden =  
 Burden of therapy for patients
 Hospitalisation
 Surgery
 Health-related quality of life
 Economic productivity
 Social functioning
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12
Q

What are the 2 types of IBD?

What are their characteristics?

A

Ulcerative colitis (UC):

Inflammatory disorder limited to the colonic mucosa

Superficial

Continuous

Always involves the rectum

Affects males and females equally
No granulomas

Crohn’s disease (CD):

Can affect any part of the GI tract - anywhere from the mouth to the anus

Deep ulcerations and deep involvement of the mucosa

Patchy chronic transmural granulomatous inflammation (patchy = different segments of the colon)

Tendency to form fistula or strictures - strictures = fibrous, stiff tissue due to exposure to severe inflammation

Females more affected than males (1.5:1)

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13
Q

What are the main differences of UC vs CD?

A

UC vs CD

Continuous vs patchy
Superficial vs deep inflammation / penetration
Always involves rectum vs any part of digestive tract but often segments of the small and large intestine

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14
Q

Can type of IBD change?

A

Yes, patients can present with UC, then CD, and they can switch between them

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15
Q

What are the different types of UC?

A

Always involves the rectum

Proctitis = only rectum

Protosigmoiditis = rectum and sigmoid

Distal colitis = rectum, sigmoid and descending colon

Extensive colitis = rectum, sigmoid, descending and transverse colon

Pancolitis = rectum, sigmoid, descending, transverse, ascending, caecum, and appendix

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16
Q

What are the different types of CD?

A

Patchy = combination of different segments of the colon

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17
Q

What are the symptoms of IBD?

A

They depend on the side of inflammation:

Collitis = bleeding, mucus, urgency to pass stool, diarrhoea

Perianal (CD only) = anal pain, leakage, difficulty passing stool

Small bowel disease (CD only) = symptoms relate to lack of absorption of nutrients = abdominal pain, weight loss, tiredness / lethargy, diarrhoea, abdominal mass

18
Q

Why does IBD present at sites outside of the colon / GI tract?

A

As it is an autoimmune condition - can affect other sites

19
Q

What are some extra-intestinal manifestations of IBD?

A

Arthritis =
Axial – Ankylosing Spondylitis
Peripheral

Skin =
Erythema nodosum
Pyoderma gangrenosum

Eyes =
Anterior uveitis
Episcleritis/Iritis

Liver =
Primary Sclerosing Cholangitis (PSC)
Autoimmune hepatitis

20
Q

What causes IBD?

A

Still unknown

A final common pathway that reflects a combination of an impaired mucosal immune response to the gut microbiota in a genetically susceptible host = in certain patients, the immune system responds inappropriately to the gut microbiota

21
Q

What factors contribute the development of IBD?

A

Genetic susceptibility = NOD2, HLA, ATG, Il23R

Immune response = anti-saccaromyces cervisiae (ASCA) - Crohn’s; pANCA - UC

Environmental factors = diet, mycobacterium paratuberculosi, MMR?

22
Q

Why does diet affect the development of IBD?

A

Diet affects gut microbiota

Results in dysbiosis i.e. unhealthy gut microbiota

23
Q

Why factors can be protective to developing IBD?

Why do patients with appendectomy not develop UC but can develop CD?

A

Physically active
Those who have and appendectomies do not get UC
Oddly, smoking - patients who stop smoking can develop IBD, although smoking worsens IBD once it develops

Apprendix = holds many of the gut microbiota

24
Q

What are the risk factors for developing a poor, unbalanced microbiota?

How does a poor, unbalanced gut microbiota affect IBD development?

A 
Lack of vitamin D exposure
Overly hygienic 
Stress
Genetic susceptibility
Gut microbiome 
Medications - e.g. antibiotics 
Poor diet
Appendectomy - develop CD, never UC

All can contribute to development of poor and unbalanced gut microbiota, which then triggers immune response leading to autoimmunity, allergy and metabolic disorders

25
Q

What are the goals of IBD management?

A

Induce clinical remission

Maintain clinical remission

Improve patient quality of life

Heal mucosa

Decrease hospitalisation/ surgery & overall cost

Minimise disease and therapy related complications

26
Q

What are the main medications used for the management of IBD?

A

Steroids

5 ASA - 5 amino salicylic acids

Immune suppressants e.g. azathioprine, methotreaxate

Biologic therapies

Others – diet, FMT, antibiotics, probiotics, novel agents

27
Q

Why are steroids used to treat IBD?

How do they work, how are they given to patients and how are they used?

A

Steroids diffuse and bind in nucleus to Glucocorticoid Responsive Elements (GRE)
GREs interact with specific DNA sequences to:
Increase anti-inflammatory gene products
Block pro-inflammatory genes

Mode of Delivery = IV, oral or rectal enemas

They are usually used:
As a bridge to other therapy/interventions
In acutely unwell patients - induce healing
Steroids stop working in the long-term, so only useful short term
Steroids also have side effects with long term use - musculoskeletal, endocrine, psychological etc.

28
Q

Why are 5 ASAs used?

How do they work and how are they given to patients?

A

Main action = inhibition of pro-inflammatory cytokines (IL-1 and TNF-a )

Inhibition of the lipo-oxygenase pathway i.e. prostaglandin and leukotrienes

Scavenging of free radicals

Inhibition of NF-kB/ TLR via PPAR-gamma induction (perioxisome proliferator activated receptor-gamma)

Some immunosuppresive activity – inhibiting T cell proliferation, activation and differentiation

Impairs neutrophil chemotaxis and activation

Mode of Delivery = orally or rectal

29
Q

What are the side effects of 5 ASA?

A 
Intolerance
Diarrhoea
Renal impairment
Headache
Malaise
Pancreatitis
Pneumonitis
30
Q

Why is the immunosuppressor azathioprine used?

How does it work?

A

Lessens immune function - suppresses the immune reaction / inflammation in IBD

6-TG is the active metabolite of Azathioprine i.e. AZA –> 6-MP –> 6TMP –>6-TG

6-TG interferes with adenine and guanine ribonucleotide production

Results in reduced number of B and T lymphocytes, immunoglobulins and interleukins

Another pathway potentially results in apoptosis of T cells

31
Q

What is checked in patients before administering azathioprine and why?

A

AZA (azathioprine)–> 6MP

6MP can then either be converted by the TPMT enzyme to 6-MMP, or it can be converted to 6-TG by the MPRT enzyme

So the TPMT enzyme is checked in all patients - if it is low, majority of the aza is coverted to 6-TG

6-TG is the active component of immunosuppression

So before starting a patient on Azathioprine, it is important to check their TMPT funciton as if it is high, they could develop serious side effects from 6-MMP (which is hepatotoxic)

32
Q

What are the side effects of Azathioprine?

A 
Second malignancies - skin cancer, lymphoma
Bone marrow suppression
Pancreatitis
Infection 
Hepato-toxicity 
Allergic reactions
33
Q

What is checked in IBD patients being given Azathioprine?

A 
Thiopurine Methyltransferase (TPMT)
Hep B/C
HIV
Chicken pox
Vaccinations
TB
Frequent bloods on starting
Maintenance bloods

These diseases can be reactivated with that level of immunosuppression - often given anti-virals for hep b/c reactivation

34
Q

How does methotrexate work?

A

Mechanism not clear
Interferes with DNA synthesis & cell reproduction
Increased adenosine levels (anti-inflammatory)
Increased apoptosis of peripheral T cells

Takes around 3 months to work

35
Q

How should the drug be delivered and monitored?

What can be given to help reduce side effects?

A

Weekly dose - need history re liver abnormalities, need to monitor LFTs, FBC

Advised not to be taken during pregnancy

Folic acid supplements (reduces side effects)

36
Q

What are the side effects of methotrexate?

A 
Rash
Nausea, mucositis
Diarrohea
Bone marrow suppression
Hypersensitivity pneumonitis
Increased liver enzymes
Hepatic fibrosis/cirrhosis
Known abortifacient (causing abortion)
No documented increased risk of lymphoma or skin cancer
37
Q

What biologic durgs ar used to treat IBD?

A

TNF-alpha is the main pathway involved in IBD, therefore anti-TNF-a is used – infliximab, adalimumab

Anti- α4β7 Vedolizumab

Anti-IL12/IL23 Ustekinumab

More on the way to being discovered / developed

38
Q

How are infliximad and adalimunab administered to patients?

A

IV - infliximab
in hospital – less frequent
Induction 0,2,6 weeks
Maintenance 8 weekly

subcutaneous injection - adalimumab (humira)
160/80/ 40mg EOW
At home – more frequent

39
Q

What are the side effects of biologics?

A 
Opportunistic infections
Infusion or site reactions
Infusion reactions
Neutropenia
Infections
Demyelinating disease
Heart failure (HF)
Cutaneous reactions, including psoriasis
Malignancy
Induction of autoimmunity
40
Q

How is IBD managed clinically?

A

Combination therapy = AZA/ 6MP and aTNF act synergistically

Combination is superior in inducing and maintaining response and remission

Reduces the rate of antibody formation

Other medications =
Cilosporin
Vedolizumab (anti-integrin)
Ustekinemab (anti IL12/23)

41
Q

What other considerations can be made when managing IBD?

A 
Dietary therapy =
Liquid therapy diet
Increased use in children
As effective as steroids
Use in small bowel Crohns disease
Weeks

Antibiotics =
No hard evidence
Good for sepsis

Faecal Microbiota Transplantation (FMT) =
Lots research into the role of the microbiome

Novel agents

Y2 - BRS - GI (14 decks)

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