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Z YEAR 2 BRS GASTRO > Lower GI Tract > Flashcards

Lower GI Tract Flashcards

1
Q

What are the different parts of the large intestine?

A
  1. Appendix
  2. Caecum
  3. Ascending colon
  4. Transverse colon
  5. Descending colon
  6. Sigmoid colon
  7. Rectum
  8. Anus
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2
Q

What is the parasympathetic innervation of the colon?

A
  1. Ascending colon + most of transverse colon innervated by vagus nerve
  2. More distal innervated by pelvic nerves
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3
Q

What is the sympathetic innervation of the colon?

A

1, lower thoracic

2. upper lumbar spinal cord

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4
Q

What is the external anal sphincter controlled by?

A

somatic motor fibres in the pudendal nerves

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5
Q

What do afferent sensory neurons detect?

A

pressure

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6
Q

What is Hirschsprung’s disease?

A

no enteric intramural ganglia

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7
Q

Where is the myenteric plexus ganglia concentrated?

A

below taenia coli

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8
Q

What are inflammatory lower GI tract disorders?

A
  1. Inflammatory Bowel Disease (IBD)

2. Microscopic colitis

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9
Q

What are infective lower GI tract disorders?

A
  1. C Diff

2. E Coli .. etc

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10
Q

What are structural lower GI tract disorders?

A
  1. Diverticular disease
  2. Haemorrhoids
  3. Fissures
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11
Q

What are functional lower GI tract disorders?

A

irritable bowel syndrome

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12
Q

What are neoplastic lower GI tract disorders?

A
  1. Colonic polyps

2. Colon cancer

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13
Q

What are other lower GI tract disorders?

A
  1. Neurological
  2. Metabolic
  3. Vascular
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14
Q

How many people are affected by Inflammatory bowel disease?

A

•Affects 1.5 million people in America and 2.2 million in
Europe

  • Several hundred thousand more worldwide
  • Lifelong chronic disease, often affecting young people
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15
Q

What is the toll of inflammatory bowel disease?

A
  1. Burden of therapy for patients
  2. Hospitalisation
  3. Surgery
  4. Health-related quality of life
  5. Economic productivity
  6. Social functioning
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16
Q

What is Ulcerative Colitis (UC)?

A
  1. Inflammatory disorder limited to the colonic mucosa
  2. Superficial
  3. Continuous
  4. Always involves the rectum
  5. M = F
  6. NO granulomas
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17
Q

What is Crohn’s disease (CD)?

A
  1. Can affect any part of the gastrointestinal tract
  2. Patchy chronic transmural granulomatous inflammation
  3. Tendency to form fistula or strictures
  4. F>M (1.5:1)
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18
Q

What are the types of ulcerative colitis?

A
  1. Procititis
  2. Poctosigmoiditis
  3. Distal colitis
  4. Extensive colitis
  5. Pancolitis
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19
Q

What are the types of Crohn’s disease?

A
  1. Ileocolitis
  2. Ileitis
  3. Gastroduodenal Crohn’s disease
  4. Jejunoiletitis
  5. Crohn’s (granulomatous) colitis
  6. perianal Crohn’s
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20
Q

What are the symptoms of colitis inflammatory bowel disease?

A
  1. Bleeding
  2. Mucus
  3. Urgency
  4. Diarrhoea
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21
Q

What are the symptoms of perianal inflammatory bowel disease?

A
  1. Anal pain
  2. Leakage
  3. Difficulty passing stool
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22
Q

What are the symptoms of small bowel disease inflammatory bowel disease?

A
  1. Abdominal pain
  2. Weight loss
  3. Tiredness/lethargy
  4. Diarrhoea
  5. Abdominal mass
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23
Q

What are the arthritis extra-intestinal manifestation of inflammatory bowel disease?

A
  • Axial – Ankylosing Spondylitis

* Peripheral

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24
Q

What are the skin extra-intestinal manifestation of inflammatory bowel disease?

A
  • Erythema nodosum

* Pyoderma gangrenosum

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25
Q

What are the eyes extra-intestinal manifestation of inflammatory bowel disease?

A
  • Anterior uveitis

* Episcleritis/Iritis

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26
Q

What are the liver extra-intestinal manifestation of inflammatory bowel disease?

A
  • Primary Sclerosing Cholangitis (PSC)

* Autoimmune hepatitis

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27
Q

What are the reasons for inflammatory bowel disease?

A
  • Genetic susceptibility
  • Luminal microbes: environmental factors
  • Immune response
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28
Q

What are the genes thought to be involved in inflammatory bowel disease?

A
  1. NOD2
  2. HLA
  3. ATG
  4. Il23R
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29
Q

What are the luminal microbe theories for inflammatory bowel disease?

A

Other theories:

  • Mycobacterium paratuberculosi
  • MMR???
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30
Q

What are the immune response reasons for inflammatory bowel disease?

A
  1. Anti-saccaromyces cervisiae (ASCA)- Crohn’s

2. pANCA – UC

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31
Q

What are the management aims of inflammatory bowel disease?

A
  1. Induce clinical remission
  2. Maintain clinical remission
  3. Improve patient quality of life
  4. Heal mucosa
  5. Decrease hospitalisation/ surgery & overall cost
  6. Minimise disease and therapy related complications
32
Q

What are the medical options for inflammatory bowel disease management?

A
  1. Steroids
  2. 5 ASA
  3. Immune suppressants
  4. Biologic therapy
  5. Others –diet, FMT, antibiotics, probiotics, novel agents
33
Q

What are the immune suppressants needed for management in inflammatory bowel disease management?

A
  • Azathioprine

* Methotreaxate

34
Q

What is the point of using steroids for management of inflammatory bowel disease?

A

Diffuse and bind in nucleus to Glucocorticoid Responsive Elements (GRE)

35
Q

How do the steroids used for the management of inflammatory bowel disease work?

A
  1. GRE interact with specific DNA sequences
  2. Increase anti-inflammatory gene products
  3. Block pro-inflammatory genes
36
Q

What is the mode of devilry for the management of inflammatory bowel disease?

A
  1. IV
  2. Orally
  3. Rectal enemas
37
Q

When do people use steroids for the management of inflammatory bowel disease?

A
  • Short term
  • As a bridge to other therapy/interventions
  • In acutely unwell patients
38
Q

When do adverse effects of steroids happen?

A
  • Prolonged use of high doses

- Cushing’s disease

39
Q

What are the psychiatric adverse effects of steroids?

A
  • sleep disturbance / activation
  • mood disturbance
  • psychosis
40
Q

What are the skin/soft tissue adverse effects of steroids?

A
  • Cushingoid appearance
  • Abdominal striae
  • Acne
  • Hirtuism
  • Oedema
41
Q

What are the neurologic adverse effects of steroids?

A
  • neuropathy

- pseudomotor cerebri

42
Q

What are the cardiovascular adverse effects of steroids?

A

hypertension

43
Q

What are the MSK adverse effects of steroids?

A
  • osteoporosis
  • asceptic necrosis of bone
  • myopathy
44
Q

What are the endocrine adverse effects of steroids?

A
  • diabetes mellitus

- adrenal cortex suppression

45
Q

What are the immunologic adverse effects of steroids?

A
  • lymphocytopenia
  • immunosuppresion
  • false-negative skin test
46
Q

What are the ophthalmic adverse effects of steroids?

A
  • cataract

- narrow-angle glaucoma

47
Q

What are the developmental adverse effects of steroids?

A

growth retardation

48
Q

What does 5 ASA do for the management of inflammatory bowel disease ?

A
  1. Inhibition of pro-inflammatory cytokines (IL-1 and TNF-a )
  2. Inhibition of the lipo-oxygenase pathway i.e. prostaglandin and leukotrienes
  3. Scavenging of free radicals
  4. Inhibition of NF-kB/ TLR via PPAR-gamma induction (perioxisome proliferator activated receptor-gamma)
  5. Some immunosuppresive activity – inhibiting T cell proliferation, activation and differentiation
  6. Impairs neutrophil chemotaxis and activation
49
Q

What is the mode of delivery for 5 ASA?

A

Orally or rectal

50
Q

What are the side effects of 5 ASA?

A
  1. Intolerance
  2. Diarrhoea
  3. Renal impairment
  4. Headache
  5. Malaise
  6. Pancreatitis
  7. Pneumonitis
51
Q

How does azathioprine work?

A
  1. 6-TG interferes with adenine and guanine ribonucleotide production
  2. Results in reduced number of B and T lymphocytes, immunoglobulins and interleukins.
  3. Another pathway potentially results in apoptosis of T cells
52
Q

What are the side effects of azathioprine?

A
  1. Allergic reaction: feverm rash, arthralgias, myalgias, fatigue
  2. GI disturbances
  3. Hepatoxicity, nodular regenerative hyperplasia
  4. Infection
  5. Pancreatitis
  6. Bone marrow suppression
  7. Malignancy / lymphoma
53
Q

What do you need to monitor when taking azathioprine?

A
  1. Thiopurine Methyltransferase (TPMT)
  2. Hep B/C
  3. HIV
  4. Chicken pox
  5. Vaccinations
  6. TB
  7. Frequent bloods on starting
  8. Maintenance bloods
54
Q

What is the mechanism of methotrexate?

A
  • Mechanism not clear
    1. Interferes with DNA synthesis & cell reproduction
    2. Increased adenosine levels (anti-inflammatory)
    3. Increased apoptosis of peripheral T cells
55
Q

How long does it take for methotrexate work?

56
Q

What do you need to monitor and check when taking methotrexate?

A
  1. Need history re liver abnormalities
  2. Monitor LFTs, FBC
  3. Advise NO pregnancy
  4. Folic acid supplements (reduces side effects)
  5. WEEKLY DOSE
57
Q

What are the side effects of methotrexate?

A
  1. Rash
  2. Nausea, mucositis, Diarrohea
  3. Bone marrow suppression
  4. Hypersensitivity pneumonitis
  5. ↑’ed liver enzymes
  6. Hepatic fibrosis/cirrhosis
  7. Known abortifacient
  8. No documented ↑ed risk of lymphoma or skin cancer
58
Q

What are some biologics?

A
  • Anti-TNFα – infliximab, adalimumab
  • Anti- α4β7 Vedolizumab
  • Anti-IL12/IL23 Ustekinumab
  • More and more on the way
59
Q

When is IV infliximab used?

A
  • in hospital – less frequent
  • Induction 0,2,6 weeks
  • Maintenance 8 weekly
60
Q

When is subcutaenous adalimumab (humira) given?

A
  • 160/80/ 40mg EOW

* At home – more frequent

61
Q

How is golimumab given (biologic)?

62
Q

What are the side effects of biologics?

A
  1. Opportunistic infections
  2. Infusion or site reactions
  3. Infusion reactions
  4. Neutropenia
  5. Infections
  6. Demyelinating disease
  7. Heart failure (HF)
  8. Cutaneous reactions, including psoriasis
  9. Malignancy
  10. Induction of autoimmunity
63
Q

What is combination therapy for inflammatory bowel disease?

A
  1. AZA/ 6MP and aTNF act synergistically
  2. Combination is superior in inducing and maintaining response and remission
  3. Reduces the rate of antibody formation
64
Q

What are other medications for inflammatory bowel disease?

A
  • Cilosporin
  • Vedolizumab (anti-integrin)
  • Ustekinemab (anti IL12/23)
65
Q

What are some other considerations for the management of inflammatory bowel disease?

A
  1. Dietary therapy
  2. Antibiotics
  3. Faecal microbiota transplantation (FMT)
  4. Novel agents
66
Q

What is the dietary therapy?

A
  • Liquid therapy diet
  • Increased use in children
  • As effective as steroids
  • Use in small bowel Crohns disease
  • Weeks
67
Q

What are the antibiotic considerations?

A
  • No hard evidence

* Good for sepsis

68
Q

What are the faecal microbiota transplantation (FMT) considerations?

A

Lots research into the role of the microbiome

69
Q

What is the difference between CD and UC?

A
  1. CD and UC have specific diagnosing characteristics and clinical outcomes
  2. e.g. diffuse vs patchy , stricture and fistula formation in CD
70
Q

How does inflammatory bowel disease manifest?

A
  • A final common pathway that reflects a combination of an impaired mucosal immune response to the gut microbiota in a genetically susceptible host
  • unhealthy and healthy microbiota not balanced and immune system react inappropriately
71
Q

What else affects inflammatory bowel disease?

A
  • Lifestyle e.g. sugary diet
  • Meidcations
  • Smoking (nicotine)
  • affects microbiota
  • causes dysbiosis
72
Q

What is dysbiosis?

A

unhealthy gut microbiota

73
Q

What doe TNF alpha do to macrophages?

A
  1. Increase pro-inflammatory cytokines
  2. Increase chemokines
    - Leads to increased inflammation
74
Q

What doe TNF alpha do to endothelium?

A
  1. Increases adhesion molecules

- Leads to increased cell infiltration

75
Q

What doe TNF alpha do to fibroblasts?

A
  1. Increases acute phage response
    - Leads to increase CRP in serum
  2. Increases metalloproteinase synthesis
  3. Decreases collagen synthesis
    - Leads to tissue remodelling
76
Q

What doe TNF alpha do to epithelium?

A
  1. Increases io transport
  2. Increase permeability
    - Leads to compromised barrier function

Z YEAR 2 BRS GASTRO (15 decks)

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