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Gastrointestinal System > Week 4 > Flashcards

Week 4 Flashcards

1
Q

The small and large intestine peristalsis is mediated by which types of neural control?

A

intrinsic (myenteric plexus)
extrinsic (autonomic innervation)

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2
Q

The myenteric plexus is composed of which nerve plexuses? and where are they located?

A
  • Meissener’s plexus: base of the submucosa.
  • Auerbach plexus: between the inner circular and outer longitudinal layers of the muscularis propria.
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3
Q

Inflammatory bowel disease is a pathological feature of which conditions?

A
  • ulcerative colitis.
  • Crohn’s disease.
  • ischaemic colitis.
  • radiation colitis.
  • appendicitis.
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4
Q

what causes IBD? (not what conditions but the actual mechanism)

A
  • strong immune response against normal flora with defects in the epithelial barrier function in genetically susceptible individuals.
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5
Q

what areas can Crohn’s disease affect?

A

any part of the GIT from the mouth to the anus

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6
Q

what gene mutation is seen in association with Crohn’s disease?

A

NOD2

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7
Q

what gene mutation is seen in association with ulcerative colitis?

A

HLA

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8
Q

what is the role of intestinal flora in the pathology of IBD?

A
  • defects in mucosal barrier could allow microbes access to mucosal lymphoid tissue triggering immune response.
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9
Q

the pANCA is present in what % of ulcerative colitis patients?

A

75%

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10
Q

the pANCA is positive in what % of Crohn’s disease patients?

A

11%

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11
Q

ulcerative colitis (UC) definition

A

a chronic relapsing-remitting inflammatory disease that primarily affects the large bowel.

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12
Q

what two peak age groups does UC most commonly occur?

A

20-30 years
70-80 years

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13
Q

features of ulcerative colitis?

A
  • continuous pattern of inflammation-
  • rectum to proximal large bowel.
  • pseudopolyps.
  • ulceration.
  • serosal surface minimal or no inflammation.
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14
Q

what will a biopsy show in UC?

A
  • loss of goblet cells, crypt abscess and inflammatory cells (predominantly lymphocytes).
  • NO GRANULOMAS.
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15
Q

what is pancolitis?

A

Pancolitis is a form of ulcerative colitis that affects the entire large intestine or bowel.

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16
Q

what are complications of uclerative colitis?

A
  • if pancolitis > 10 years > 20-30x higher risk of developing cancer.
  • haemorrhage.
  • perforation.
  • toxic dilatation.
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17
Q

in what two age groups does Crohn’s disease peak in?

A

20-30 years
60-70 years

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18
Q

what will a colonoscopy with biopsy of Crohn’s disease reveal?

A
  • intermittent inflammation (‘skip lesions’).
  • cobblestone mucosa (due to ulceration and mural oedema).
  • rose-thorn ulcers (due to transmural inflammation) +/- fistulae or abscesses.
  • non-caseating granulomas.
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19
Q

what are long-term features of crohn’s disease?

A
  • small intestine malabsorption > malnutrition.
  • strictures.
  • fistulas and abscesses.
  • perforation.
  • increased risk of cancer 5x.
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20
Q

NESTS mnemonic in differentiating features of CD from UC

A
  • No blood or mucus (less common).
  • Entire GI tract affected.
  • Skip lesions, strictures and fistulas.
  • Terminal ileum most affected and transmural (full thickness) inflammation.
  • Smoking is a risk factor.
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21
Q

CLOSEUP mnemonic in differentiating between UC and CD

A
  • Continuous inflammation.
  • Limited to the colon and rectum.
  • Only superficial mucosa affected.
  • Smoking may be protective.
  • Excrete blood and mucus.
  • Use aminosalicylates.
  • Primary sclerosing cholangitis.
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22
Q

What is ischaemic enteritis?

A

inflammation of the small or large intestine or both due to blood vessel occlusion.

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23
Q

describe appendicitis?

A
  • inflammation of the appendix.
  • typically develops due to an obstruction within the appendix.
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24
Q

what are complications of appendicitis?

A
  • tissue damage.
  • pressure-induced necrosis.
  • perforation.
  • gangrene due to thrombosis in ileocolic artery.
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25
Q

what is a dysplasia of the large bowel also called?

A

adenoma (‘polyp’)

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26
Q

What are the risk factors in developing colorectal adenocarcinoma?

A
  • lifestyle
  • family history
  • IBD: UC and CD
  • Genetics: FAP, HNPCC, Peutz-Jeghers.
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27
Q

what are clinical features of right-sided adenocarcinoma of colon?

A
  • exophytic/polypoid (grows outwards from epithelium).
  • anaemia (chronic bleeding).
  • vague pain.
  • weakness.
  • obstruction.
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28
Q

what are features of left-sided colorectal adenocarcinoma?

A
  • annular (ring-shaped) > napkin ring lesion.
  • bleeding > fresh/altered blood PR.
  • altered bowel habit.
  • obstruction.
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29
Q

what side of the large intestine is the site of most bacterial fermentation?

A

right-side

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30
Q

what are the three main short-chain fatty acids produced by microbial fermentation in the large intestine? and how are they used locally?

baby please aaaaa

A
  • butyrate
  • propionate
  • acetate
  • energy source for gut eptihelial cells.
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31
Q

what is the function of butyrate

A

epithelial cell growth and regeneration

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32
Q

what is the function of propionate?

A

gluconeogenesis in the liver
satiety signalling

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33
Q

what is the function of acetate?

A

transported in blood to peripheral tissues > lipogenesis

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34
Q

what is the significance of the pH of the proximal colon?

A

low pH of 5.5
inhibits pathogems who generally grow optimally at pHs over 6

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35
Q

what are the two methods of colonisation resistance in the large intestine?

A
  1. barrier effect
  2. active competitive exclusion
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36
Q

Describe the barrier effect of colonisation resistance in the large intestine

A
  • the large numbers of the indigenous microbiota prevent colonisation by ingested pathogens and inhibit overgrowth of potentially pathogenic bacteria normally resident at low levels.
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37
Q

dysbiosis of the gut microbiota has been linked to which central nervous system conditions?

A

autistic spectrum disorder
major depressive disorder
multiple sclerosis

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38
Q

dysbiosis of the gut microbiota has been linked to which metabolic disorders?

A

insulin resistance (T2D)
metabolic syndrome
obesity
CVD

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39
Q

what are the consequences of antibiotic exposure to the gut microbiota?

A
  • loss of bacterial diversity > opportunity for pathogen colonisation by C.difficile for example which produces toxins.
  • bacterial resistance
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40
Q

how does fecal microbiotic transplantation (FMT) work? What can it be used to treat?

A
  • faecal sample from screened healthy donor transplanted into recipient with dysbiosis.
  • Donor microbiota repopulates large intestine, displaces C.difficile, prevents reinfection.
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41
Q

summarise the role of bacteria in the large intestine

A
  • ferment dietary fibre.
  • produce metabolites to communicate with other bacteria and the host.
  • prime the immune system.
  • prevent pathogen colonisation.
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42
Q

what external influences can affect the gut microbiota?

A

diet
antibiotics
probiotics
symbiotic
prebiotics
ageing
disease

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43
Q

del

A

del

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44
Q

what are clinical features of IBS?

A
  • abdominal pain > improvement with defecation.
  • altered bowel habit.
  • abdominal bloating.
  • belching wind and flatus.
  • passage of mucus.
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45
Q

why do we test for calprotectin in stool samples?

A
  • calprotectin is released by inflamed gut mucosa.
  • used for differentiating between irritable bowel disease and inflammatory bowel disease.
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46
Q

what does treatment for IBS consist of?

A
  • dietary review > cut out irritants.
  • drug therapy to treat symptoms:
    > painkillers or antidepressants for pain.
    > probiotics for bloating.
    > laxatives for constipation.
    > antimotility agents, FODMAP for diarrhoea.
  • PSYCHOLOGICAL INTERVENTIONS.
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47
Q

some causes for IBS?

A
  • altered motility.
  • visceral hypersensitivity.
  • stress, anxiety, depression.
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48
Q

describe changes in intestinal motility seen in IBS-D and IBS-C

A

In IBS-D, muscular contractions may be stronger and more frequent than normal.
In IBS-C, contractions may be reduced.

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49
Q

what is inflammatory bowel disease?

A

chronic, relapsing, remitting inflammation of GI tract.
e.g. CD and UC

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50
Q

del

A

del

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51
Q

what are symptoms of UC?

A

bloody diarrhoea
abdominal pain
weight loss
fatigue

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52
Q

what is proctitis?

A

inflammation of the rectum

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53
Q

what are investigations for suspected UC?

A
  • bloods for markers of inflammation- normocytic/microcytic anaemia:
    > ^CRP/WCC/Platelets
    > decreased albumin.
  • stool culture to rule out infection.
  • faecal caprotectin > 200ug/g is elevated.
  • colonoscopy and colon mucosal biopsies.
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54
Q

what will a colonoscopy of UC reveal?

A

continuous inflammation
erythematous mucosa
loss of haustral markings
pseudopolyps

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55
Q

what will a barium enema of UC reveal?

A
  • lead-piping inflammation (secondary to loss of haustral markings).
  • thumb-printing (a marker of bowel wall inflammation).
  • pseudopolyps.
56
Q

outline the management of acute, severe UC

A
  1. IV corticosteroids first-line.
  2. IV ciclosporin.
  3. infliximab (Anti-TNF antibody)
  4. Surgery
57
Q

what are short-term/acute complications in UC?

A

Toxic megacolon
massive lower GI haemorrhage.

58
Q

what are long-term complications of UC?

A

Colorectal cancer
cholangiocarcinoma
colonic strictures
primary sclerosing cholangitis
inflammatory pseudopolyps

59
Q

investigation CD

A
  • bloods > CRP, WCC etc.
  • stool culture
  • faecal calprotectin
  • endoscopy with imaging required for diagnosis.
  • MRI for suspected small bowel disease.
  • colonoscopy with biopsy.
60
Q

what are symptoms of CD?

A

symptoms:
- GI symptoms > crampy abdominal pain and diarrhoea.
- systemic symptoms > weight loss and fever.

61
Q

what are signs of CD?

A
  • cachexia.
  • paleness (anaemia).
  • mouth ulcers.
  • abdominal/right lower quadrant tenderness and a right iliac fossa mass.
  • perirectal examination may have skin tags, fistulae or perianal abscess.
62
Q

what are the symptoms of perianal crohn’s disease?

A

perianal pain
pus secretion
unable to sit down

63
Q

investigations for perianal crohn’s disease?

A

MRI pelvis
Examination under anaesthetic (EUA)

64
Q

treatment for perianal Crohn’s disease?

A
  • surgery to drain abscess and place seton stitch.
  • antibiotics.
  • biological therapy (anti-TNF).
65
Q

What are some extra-intestinal manifestations of IBD?

A
  • mouth ulcers
  • skin: erythema nodosum, pyoderma gangrenosum.
  • eyes: anterior uveitis, episcleritis, scleritis.
  • musculoskeletal: arthritis, sacro-ilitis, ankolysing spondalitis.
  • primary sclerosing cholangitis.
66
Q

discuss the treatment of mild to moderate acute UC

A
  • aminosalicylate (e.g., oral or rectal mesalazine) first-line.
  • corticosteroids (e.g., oral or rectal prednisolone) second-line
67
Q

how do aminosalicylates treat UC?

A

blocking prostaglandins and leukotrienes

68
Q

what is the treatment for maintaining remission in UC?

A
  • aminosalicylate (mesalazine) first-line.
  • azathioprine.
  • mercaptopurine.
69
Q

discuss the surgical management of UC

A

Removing the entire large bowel and rectum (panproctocolectomy) will remove the disease. The patient has either a permanent ileostomy or an ileo-anal anastomosis (J-pouch).

70
Q

how is an exacerbation of Crohn’s disease treated?

A
  • steroids (e.g., oral prednisolone 40mg or IV hydrocortisone) first-line.
  • enteral nutrition as an alternative.

other meds if steroids dont work:
azathioprine
mercaptopurine
methotrexate
infliximab (anti-TNF antibodies)
adalimumab (anti-TNF antibodies)

71
Q

what is the treatment for maintaining remission in CD?

A

first-line:
azathioprine
mercaptopurine

or methotrexate

72
Q

what are indications for emergency surgery in acute IBD?

A
  1. acute severe colitis not responding to high dose IV steroids =/- anti-TNF biologic ‘rescue’ therapy.
  2. Complications such as perforation, obstruction and abscess.
73
Q

indications for elective surgery for IBD

A
  1. frequent relapses despite medical therapy.
  2. not able to tolerate medical therapy.
  3. steroid dependent patients.
74
Q

surgical options for CD?

A
  • resection of distal ileum when the disease is isolated to this area.
  • treating strictures.
  • treating fistulas.
75
Q

what is the overall mortality of acute GI bleeding in the UK?

A

7%

76
Q

what is the mortality rate if acute GI bleeding in patients admitted to hospital for other reasons?

A

26%

77
Q

what features is upper GI bleeding associated with?

A
  • haematemesis (vomiting fresh blood).
  • melaena (black stools).
  • elevated urea (partially digested blood > haem > urea).
  • associated with dyspepsia, reflux, epigastric pain.
  • NSAID use.
78
Q

what features are associated with lower GI bleeding?

A
  • fresh blood/clots.
  • magenta stools.
  • normal urea (rarely elevated in proximal small bowel).
  • typically painless.
  • more common in advanced age.
79
Q

what are some oesophageal causes of upper GI bleeding?

A
  • ulcer
  • oesophagitis
  • varices
  • Mallory Weiss tear
  • malignancy
80
Q

what are some gastric causes of upper GI bleeding?

A
  • ulcer
  • gastritis
  • varices
  • malignancy (may be under an ulcer)
  • Dieulafoy lesion
  • angiodysplasia (tends to be chronic)
81
Q

what are some duodenal causes of upper GI bleeding?

A
  • ulcer
  • duodenitis
  • angiodysplasia (tends to be chronic)
82
Q

what are the top five most common causes of an acute upper GI bleed?

A
  1. gastric cancer
  2. duodenal ulcer
  3. mallory-weiss tear
  4. oesophagitis
  5. oesophageal varices
83
Q

are duodenal or gastric ulcers more common?

A

duodenal (75%)

84
Q

what are risk factors in developing a peptic ulcer?

A
  • H.pylori infection
  • NSAIDs/aspirin
  • alcohol excess
  • systemic illness- stress ulcers
85
Q

how do NSAIDs cause a peptic ulcer?

A
  • COX-1 and COX-2 inhibition, and topical irritation.
  • this causes reduced blood flow, increased leukocyte adhesion and epithelial damage > mucosal injury.
86
Q

what is Zollinger-Ellison syndrome and what does it cause?

A

gastrin-secreting pancreatic tumour that causes recurrent poor healing duodenal ulcers.
tumour sits underneath ulcer.

87
Q

why does bleeding tend to occur in gastritis and duodenitis?

A

tend to bleed in context of impaired coagulation:
- medical conditions.
- anti-coagulants (warfarin, LMWH etc.).
- anti-platelets (clopidogrel, ticagrelor).

88
Q

what are some causes of oesophagitis?

A
  • reflux.
  • hiatus hernia.
  • alcohol.
  • biphosphonates (drugs used to treat osteoporosis).
  • systemic illness.
89
Q

what are the most common varices that cause GI bleeding?

A

oesophageal (90%)
gastric (8%)
rectal and spleen (rare)

90
Q

Describe a Mallory-Weiss tear

A
  • linear tear at oesophago-gastric junction
  • follows period of retching/vomiting
  • up to 10% significant requiring endoscopic treatment.
91
Q

what is a diuelafoy lesion?

A
  • a submucosal arteriolar vessel eroding through mucosa.
  • it bleeds in the absence of any abnormality.
  • usually found in gastric fundus.
92
Q

what is an angiodysplasia?

A
  • a vascular malformation that can occur anywhere in the GI tract.
  • usually causes chronic occult or overt occult bleeding.
  • associated with chronic conditions including heart valve replacement.
93
Q

what is haematemesis?

A

vomiting of blood due to active haemorrhage from the oesophagus, stomach or duodenum.

94
Q

lower GI bleeding accounts for what percentage of acute GI bleeding cases?

A

25%

95
Q

what are some causes of acute lower GI bleeding?

A
  • diverticular disease.
  • haemorrhoids.
  • vascular malformation (angiodysplasia, arteriovenous malformation).
  • neoplasia (carcinoma or polyps).
  • ischaemic colitis.
  • radiation enteropathy/proctitis.
  • IBD.
96
Q

Describe diverticular disease

A
  • protrusion of the inner mucosal lining through the outer muscular layer forming a pouch.
  • diverticulosis - presence.
  • diverticulitis - inflammation.
97
Q

what are haemorrhoids?

A
  • enlarged vascular cushions around anal canal.
  • painful if thrombosed or external.
98
Q

what are haemorrhoids associated with?

A

straining/constipation
low fibre diet

99
Q

how is angiodysplasia treated?

A

Argon phototherapy

100
Q

what is ischemic colitis? what are its complications? and what is the appearance of the mucosa?

A
  • disruption in blood supply to colon.
  • gangrene and perforation.
  • dusky blue, swollen mucosa.
101
Q

del

A
102
Q

what investigations are performed when investigating small bowel causes of acute lower GI bleeding?

A
  • CT angiogram
  • Meckel’s scan (scintigraphy) for Meckel’s diverticulum.
  • capsule endoscopy
  • double balloon enteroscopy
103
Q

when is a blood transfusion indicated in acute GI bleeding?

A

if Hb < 7g/dl or ongoing active bleeding

104
Q

describe circulatory shock

A

circulatory collapse resulting in inadequate tissue and oxygen delivery leading to global hypoperfusion and tissue hypoxia.

105
Q

what is the clinical presentation of circulatory shock caused by haemorrhage?

A
  • tachypnoea
  • tachycardia
  • anxiety or confusion
  • cool clammy skin
  • low urine output (oliguria)
  • hypotension
106
Q

what are risk stratification factors in lower GI bleeding?

A
  • age > occurs most often in elderly.
  • co-morbidity > presence of 2 co-morbid conditions doubles the chance of a severe bleed.
  • inpatients > 23% mortality compared to 3.6%.
  • initial shock.
  • drugs > NSAIDS and aspirin.
107
Q

what are the endoscopic therapy options for a peptic ulcer?

A
  • injection > adrenaline 1:10000
  • thermal > contact- ‘gold probe’
  • mechanical > clip
  • combo therapy most effective (adrenaline + thermal/clips)
108
Q

what are the management options of peptic ulcers that have ongoing bleeding and are uncontrollable endoscopically?

A
  • angiography with embolisation.
  • laparotomy.
109
Q

what are the pharmacological treatments for managing GI bleeding caused by varices?

A
  • terlipressin > vasoconstrictor of splanchnic blood supply > reduces blood flow to portal vein > reducing pressure.
  • antibiotics . often systemic infection is recipitant.
  • reverse abnormal coagulation.
110
Q

describe endoscopy with endotherapy in treating varices in different areas of GI tract

A
  • oesophageal > band ligation and glue injection.
  • gastric > glue injection.
  • rectal > glue injection.
111
Q

if varcieal bleeding is ongoing and uncontrollable endoscopically, what are the other options?

A
  • Sengstaken-Blakemore tube.
  • Transjugular intrahepatic porto-systemic shunt (TIPSS)..
112
Q

del

A

del

113
Q

how does generalised peritonitis occur?

A

represents failure of localisation and occurs when:
- contamination too rapid.
- contamination persists.
- abscess ruptures.

114
Q

what type of bacteria are highly prevalent in a peritoneal abscess?

A

anaerobes

115
Q

what conditions should be considered when investigating the acute abdomen?

A
  • peritonitis.
  • intestinal obstruction.
  • ischaemia.
  • non-surgical abdominal pain.
116
Q

what are some routes of peritonitis infection?

A
  • perforation of Gi biliary tract.
  • female genital tract.
  • penetration of abdominal wall.
  • haematogenous spread.
117
Q

what are cardinal features of intestinal obstruction?

A

depends on site (proximal vs distal) but:
pain
vomiting
distension
constipation
borborygmi (rumbling, gurgling noise)

118
Q

what questions would you ask about abdominal pain?

A
  • character: visceral, somatic, referred.
  • site of pain.
  • severity.
  • systemic upset.
119
Q

how is visceral pain transmitted?

A
  • nociceptors in smooth muscle.
  • afferent impulses run with sympathetic fibres accompanying segmental vessels (coeliac trunk, SMA, IMA).
  • poorly localised.
120
Q

describe transmission of somatic and referred pain

A
  • receptors in parietal peritoneum or abdominal wall.
  • afferent signals pass with segmental nerves (dermatomes).
  • accurate localisation but can be referred.
121
Q

what are the complications of peritonitis, ischaemia and obstruction?

A

fluid loss
sepsis
circulatory collapse
death

122
Q

acute abdomen investigations

A
  • ward tests: urine + bHCG (ectopic pregnancy).
  • lab tests: FBC, U + Es, LFTs & amylase.
  • radiology: plain, US, axial (CT) ?other.
  • laparascopy vs laparotomy
123
Q

del

A
  • restore circulating fluid volume (IV fluids).
  • enhance tissue perfusion.
  • enhance tissue oxygenation.
  • treat sepsis.
  • decompress gut.
  • ensure adequate pain relief.
124
Q

describe coeliac disease

A
  • an autoimmune condition triggered by eating gluten.
125
Q

what other autoimmune conditions are linked with coeliac disease?

A
  • type 1 diabetes.
  • thyroid disease.
  • primary biliary cholangitis.
126
Q

what is the pathophysiology of coeliac disease?

A
  • autoantibodies are created in response to exposure to gluten.
  • these autoantibodies target the epithelial cells of the small intestine, leading to inflammation.
  • inflammation affects the small intestine, particularly the jejunum.
127
Q

what antibodies are related to coeliacs?

A
  • anti TTG,
  • anti-EMA.
  • anti-DGP.
128
Q

what structural changes occur in the small intestine in coeliac disease?

A
  • atrophy of intestinal villa, resulting in malabsorption.
  • crypt hypertrophy.
129
Q

del

A

HLA-DQ2
HLA-DQ8

130
Q

what are the symptoms and signs of coeliac disease?

A
  • failure to thrive in young children.
  • diarrhoea.
  • bloating.
  • fatigue.
  • weight loss.
  • mouth ulcers.
  • dermatitis herpetiforms.
  • anaemia.
131
Q

what is dermatitis herpetiforms?

A

an itchy, blistering skin rash, typically on the abdomen, caused by coeliac disease.

132
Q

why can coeliac disease cause anaemia?

A

occurs secondary to malabsorption and deficiency of iron, B12 or folate.

133
Q

coeliac disease investigations?

A

first-line:
- total immunoglobulin A levels (to exclude IgA deficiency).
- anti-tissue transglutaminase antibodies (anti-TTG).

second-line:
- anti-endomysial antibodies (anti-EMA).

if + antibody test:
- endoscopy and jejunal biopsy showing crypt hyperplasia and villous atrophy.

134
Q

complications of coeliac disease

A
  • nutritional deficiencies.
  • anaemia.
  • osteoporosis.
  • hyposplenism.
  • ulcerative jejunitis.
  • enteropathy-associated T-cell lymphoma (EATL).
  • non-hodgkin lymhoma.
  • small bowel adenocarcinoma.
  • oesophageal carcinoma.
135
Q

what is the treatment for dermatitis herpetiforms?

A
  • gluten free diet.
  • dapsone.
136
Q

what are functional causes of vomiting?

A

pregnancy
migraine
alcohol

Gastrointestinal System (16 decks)

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