Lower GI Tract Flashcards

1
Q

Describe the basic anatomy of the Lower GI tract?

A
Appendix
Caecum
Ascending Colon
Transverse Colon
Descending Colon
Sigmoid Colon
Rectum 
Anus
Small bowel
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2
Q

What is the parasympathetic supply to the lower GI tract?

A

Ascending colon and most of transverse colon innervated by vagus nerve

More distal innervated by pelvic nerves

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3
Q

What is the sympathetic innervation of the GI tract?

A

lower thoracic and upper lumbar spinal cord

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4
Q

What is the purpose of the illiocaecal valve?

A

Gives access to the terminal illeum

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5
Q

What provides the blood supply to the lower GI tract? (Arterial)

A

Small bowel - SMA

Colon - branches of SMA and IMA (mainly left side)

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6
Q

What provides the blood supply to the lower GI tract? (Venous)

A

SMV
IMV
Both join the portal vein and eventually the inferior vena cava

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7
Q

What are the 4 layers of the gut?

A

Mucosa: Epithelium, Lamina propia and muscularis mucosae

Submucosa

Muscularis: Circular and Lpongituidinal

Serosa: Nerve supply

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8
Q

What are the nerve plexuses in the gut?

A

Myenteric plexus

Submucosal plexus

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9
Q

What is the main features of the mucosa?

A

Glands that produce mucin that lubricates the bowel making the passing of faeces easier

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10
Q

What is the nerve supply to the external anal sphincter?

A

somatic motor fibres in the pudendal nerves

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11
Q

What is the function of the afferent sensory neurons?

A

Detect pressure

Send signals to empty

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12
Q

Where is the myenteric plexus gangila?

A

Concentrated below the teniae coli?

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13
Q

What are the inflammatory bowel disorders?

A

Inflammatory bowel disease

Micrscopic colitis (normal looking mucosa, but histological abnormalities on biopsy)

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14
Q

What are some infective bowel disorders?

A

C Diff

Ecoli

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15
Q

What are some structural bowel disorders?

A

Diverticular disease
Haemorrhoids
Fissures

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16
Q

What are some functional bowel disorders?

A

Irritable bowel syndrome

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17
Q

What are some neoplastic bowel disorder?

A

Colonic polyps

Colon cancer

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18
Q

What are some other causes of bowel disorders?

A

Neurological
Metabolic
Vascular

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19
Q

How many people in Europe and America are affected by IBD?

A

1.5 million people in America and 2.2 million in Europe

Particularly high in the northern hemisphere

But more recently studies in Asia and the Middle East have shown increasing incidence world wide

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20
Q

Who does IBD often affect?

A

Often young people

Lifelong chronic disease

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21
Q

What is the toll of IBD?

A
Burden of therapy for patients
Hospitalisation
Surgery
Health-related quality of life
Economic productivity
Social functioning
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22
Q

What does IBD comprise?

A

Ulcerative Colitis

Crohn’s disease

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23
Q

What are the features of Ulcerative Colitis?

A
Inflammatory disorder limited to the colonic mucosa
Superficial
Continuous
Always involves the rectum
Only large bowel
M = F
NO granulomas
24
Q

What are the features of Crohn’s disease?

A

Can affect any part of the gastrointestinal tract
Patchy chronic transmural granulomatous inflammation
Tendency to form fistula or strictures
Affects deeper structures
Small and Large bowel
F>M (1.5:1)

25
Q

What is UC involving only the rectum?

A

Proctitis

26
Q

What is UC involving the rectum and sigmoid?

A

Proctosigmoiditis

27
Q

What is UC involving the rectum, sigmoid and descending?

A

Distal colitis

28
Q

What is UC involving the rectum, sigmoid, descending and transverse?

A

Extensive Colitis

29
Q

What is UC involving the whole large bowel?

A

Pancolitis

30
Q

What are the symptoms of Colitis?

A

Bleeding
Mucus
Urgency
Diarrhoea

31
Q

What are the perianal symptoms of perianal disease? (Crohn’s)

A

Anal pain
Leakage
Difficulty passing stool

32
Q

What are the symptoms of small bowel disease?

A
Abdominal pain
Weight loss
Tiredness/lethargy
(Caused by reduces absorption)
Diarrhoea
Abdominal mass
33
Q

What are the 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

34
Q

What causes IBD?

A

In genetically susceptible patients

They respond inappropriately to git microbiota

Imbalance between healthy and pathological microbiota

Causing inflammation

35
Q

What are the three factors of IBD aetiology?

A

Luminal microbes (environmental factors)

Genetic susceptibility

Immune respnse

36
Q

Using GWAs, which genes were found to be involved with IBD?

A

NOD2
HLA
ATG
Il23R

30+ genes now known

37
Q

What are the environmental factors?

A

Poor diet results to alteration of the microbiota

38
Q

What is dysbiosis?

A

Unhealthy gut microbiota

39
Q

Who are less likely to have IBD?

A

Physically active

Those who have and appendectomies do not get UC

40
Q

What worsens crohn’s disease?

A

Smoking
Diagnosed earlier
Worsens symptoms

Oddly protective of UC

41
Q

What are the main management goals with IBD?

A

Induce clinical remission

Maintain clinical remission

Improve patient quality of life

42
Q

What are the other management goals?

A

Heal mucosa

Decrease hospitalisation/ surgery & overall cost

Minimise disease and therapy related complications

43
Q

What treatments are used for IBD?

A

Steroids

5 ASA

Immune suppressants
Azathioprine
Methotreaxate

Biologic therapy

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

44
Q

How do steroids work?

A

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

Used short term and to induce healing in hospital settings

Significant side effects long term

Can be delivered IV, Orally or Rectally

45
Q

How does 5 Amino-Salycylic-Acids work?

A

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

Orally or rectal

46
Q

What are the sides effects of 5 ASA?

A

Intolerance

Diarrhoea

Renal impairment

Headache

Malaise

Pancreatitis

Pneumonitis

47
Q

What immunomodulator is used in IBD?

A

Azathioprine

48
Q

How does Azathroprine work?

A

6-TG interferes with adenine and guanine ribonucleotide production.

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

Reduces inflammation via suppressing immune system

Another pathway potentially results in apoptosis of T cells

49
Q

What are the side effects of Azathioprine?

A
Allergic reaction
Infection
Pancreatitis
Bone marrow surpression
GI gisturbances
Hepatotoxicity
50
Q

What is checked before giving immunosurpressants?

A
Thiopurine Methyltransferase (TPMT)
Hep B/C
HIV
Chicken pox
Vaccinations
TB
Frequent bloods on starting
Maintenance bloods
51
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 3 months to work
Need history re liver abnormalities
Monitor LFTs, FBC
Advise NO pregnancy
Folic acid supplements (reduces side effects)
WEEKLY DOSE
52
Q

What biologic drugs are used?

A

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

53
Q

What are the side effects of methotrexate?

A
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
54
Q

Give examples of how biologics are used in hospital?

A

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

s/c adalimumab (humira)
160/80/ 40mg EOW
At home – more frequent

s/c Golimumab

55
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
56
Q

What combination therapy is used in IBD?

A

AZA/ 6MP and aTNF act synergistically

Combination is superior in inducing and maintaining response and remission

Reduces the rate of antibody formation

57
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