Lower GI tract Flashcards

1
Q

what is the anatomy of the large intestine?

A
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2
Q

what are the arteries and veins of lower GI tract?

A
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3
Q

what does the inferior mesenteric artery supply?

A

left side of the colon

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4
Q

what area is under parasympathetic control?

A
  • Ascending colon and most transverse colon in innervated by vagus nerve
  • More distal innervated by pelvic nerves
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5
Q

what area is under sympathetic control?

A

lower thoracic and upper lumbar spinal cord

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6
Q

what is the external anal sphincter controlled by?

A

somatic motor fibres in pudendal nerves (S1,S2,S3)

afferent sensory neurons detect pressure- send signals for emptying of rectum

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7
Q

what does the enteric nervous system do?

A

pace maker in the bowel

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8
Q

what disease is caused by lack enteric nervous system?

A

Hirschsprung’s disease

no enteric intramural ganglia

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9
Q

where is the myenteric plexus ganglia located?

A

concentrated below taenia coli

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10
Q

what are lower GI disorders split into?

A

inflammatory

infective

structural

functional

neoplastic

other

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11
Q

what inflammatory lower GI disorders are there?

A

inflammatory bowel disease (IBD)

microscopic colitis

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12
Q

what are the infective lower GI disorders?

A

C.Diff

E. Coli

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13
Q

what are the structural lower GI disorders?

A

diverticular disease

hemorrhoids

fissures

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14
Q

what are the functional lower GI disorders?

A

irritable bowel syndrome

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15
Q

what are the neoplastic lower GI disorders?

A

colonic polyps and colon cancer

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16
Q

what are the other lower GI disorders?

A

neurological

metabolic

vascular

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17
Q

what are the subsets of inflammatory bowel disease?

A

Ulcerative colitis (UC) and Crohn’s disease (CD)

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18
Q

what are the concepts of ulcerative colitis?

A
  • Inflammatory disorder limited to the colonic mucosa
  • Superficial layer
  • Continuous
  • Always involves the rectum
  • M = F
  • NO granulomas
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19
Q

what are the types of ulcerative colitis?

A
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20
Q

what are the features of chron’s disease?

A
  • Can affect any part of the gastrointestinal tract
  • Patchy chronic transmural granulomatous inflammation
  • Tendency to form fistula or strictures
  • F>M (1.5:1)
  • Hallmark = ulceration
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21
Q

what is a fistula?

A

penetration from deep inflammation between 2 different walls

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22
Q

what is a stricture?

A

narrowing of lumen due to inflammation and oedema

form fibrous tissue that does not open up again

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23
Q

what are the types of crohn’s disease?

24
Q

what are the symptoms of UC and Crohns?

A

depends on site of inflamation

  • Colitis
    • Bleeding
    • Mucus
    • Urgency
    • Diarrhoea
  • Perianal (crohn’s disease only)
    • Anal pain
    • Leakage
    • Difficulty passing stool
  • Small bowel disease (crohn’s disease only)
    • Abdominal pain
    • Weight loss
    • Tiredness/lethargy
    • Diarrhoea
    • Abdominal mass
25
what are some extra-intestinal manifestations of IBD?
* **Arthritis** * Axial – Ankylosing Spondylitis * Peripheral * **Skin** * Erythema nodosum * Pyoderma gangrenosum * **Eyes** * Anterior uveitis * Episcleritis/Iritis * **Liver** * Primary Sclerosing Cholangitis (PSC) * Autoimmune hepatitis
26
what is the aetiology of IBD?
combination of impaired mucosal immune response to the gut microbiota in a genetically susceptible host imbalance between pathological and healthy microbiota
27
what is the genetic susceptibility to IBD?
NOD2 HLA ATG IL23R
28
what is the immune response causing IBD?
Anti-saccharomyces cervisiae (ASCA)- Crohn's pANCA-UC
29
what other environmental factors may contribute to the formation of IBD?
luminal microbes | (mycobacterium paratuberculosi)
30
what affect does diet have on IDB?
unhealthy food= change microbiota causing dysbiosis (unhealthy microbiota)
31
what is the effect of appendectomy on IBD?
protection from UC but can develop Crohn's disease (appendix is a store of microbiota)
32
what is the effect of smoking on IBD
protective against UC makes Crohn's worse
33
what is the effect of hygiene on IBD
high hygiene can develop IBD
34
what is dysbiosis?
development of poor and unbalanced bacterial communities in gut lumen pathologies= autoimmunity,allergy, metabolic disorders
35
what is the management for IBD?
* Induce clinical remission * Maintain clinical remission * Improve patient quality of life * Heal mucosa * Decrease hospitalisation/ surgery & overall cost * Minimise disease and therapy related complications
36
what drugs can be used to treat IBD?
* Steroids * 5 ASA * Immune suppressants * Azathioprine * Methotreaxate * Biologic therapy * Others –diet, FMT, antibiotics, probiotics, novel agents
37
what are the modes of delivery of steroids?
IV, orally, rectal enemas
38
how do steroids work in IBD?
* **Diffuse and bind in nucleus to Glucocorticoid Responsive Elements (GRE).** * GRE interact with specific DNA sequences * Increase anti-inflammatory gene products * Block pro-inflammatory genes `
39
what is the use of steroids in IBD?
short term as a bridge to other therapy/interventions in acutely unwell patients
40
what are the side effects of steroids?
41
what is the effect of 5 ASA?
* 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 (peroxisome proliferator activated receptor-gamma) * Some immunosuppressive activity – inhibiting T cell proliferation, activation and differentiation * Impairs neutrophil chemotaxis and activation
42
what is the mode of delivery of 5 ASA?
orally or rectally
43
what are the side effects of 5 ASA?
* Intolerance * Diarrhoea * Renal impairment * Headache * Malaise * Pancreatitis * Pneumonitis
44
how does azathioprine work?
* 6-TG (the active metabolite) 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
45
what needs to be checked before giving asathioprine?
* Thiopurine Methyltransferase (TPMT) (low in patients on this medication) * Hep B/C * HIV * Chicken pox * Vaccinations * TB * Frequent bloods on starting * Maintenance bloods
46
how does methotrexate work?
* Interferes with DNA synthesis & cell reproduction * Increased adenosine levels (anti-inflammatory) * Increased apoptosis of peripheral T cells
47
what happens when taking methotrexate?
* Takes 3 months to work * Need history re liver abnormalities * Monitor LFTs, FBC * Advise NO pregnancy * Folic acid supplements (reduces side effects) * WEEKLY DOSE
48
what are the side effects of methotrexate?
* Rash * Nausea, mucositis, Diarrohea * Bone marrow suppression * Hypersensitivity pneumonitis * ↑’ed liver enzymes * Hepatic fibrosis/cirrhosis * Known abortifacient * No documented ↑ed risk of lymphoma or skin cancer
49
what are the types of biologics that can be used?
* Anti-TNFα – infliximab, adalimumab * Anti- α4β7 Vedolizumab * Anti-IL12/IL23 Ustekinumab
50
what are the effects of TNF alpha?
51
how is infliximab delivered?
IV in hospital-less frequent induction 0,2,6 weeks maintenance 8 weekly
52
how is adalimumab delivered?
S/C 160/80/40mg Every other week at home -more frequent
53
how is golimumab delivered?
S/C
54
what are the side effects of biologics?
* Opportunistic infections * Infusion or site reactions * Infusion reactions * Neutropenia * Infections * Demyelinating disease * Heart failure (HF) * Cutaneous reactions, including psoriasis * Malignancy * Induction of autoimmunity
55
how is IBD managed?
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 mediations * Cilosporin * Vedolizumab (anti-integrin) * Ustekinemab (anti IL12/23)
56
what are other consideration treatments in IBD?
* 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