wk 3/4 GI Flashcards

1
Q

GORD symptoms

A
  • acid reflux
  • heart burn
  • waterbrash
  • often meal related
  • postural (when lying down)
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2
Q

investigations of oesophageal disease

A
  • endoscopy or biopsy
  • barium swallow test
  • oesophageal function test (manometry, pH & impendence monitoring)
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3
Q

reflux oesophagitis

A
  • Result of GORD
  • If acid stays in oesophagus long enough people can get erosions of diff. severity
  • Graded A-D depending how severe it is/ what percentage of circumference of oesophagus is occupied
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4
Q

barrett’s oesophagus

A
  • Specialised intestinal metaplasia in the lower oesophagus
  • Squamous epithelium replaced by columnar epithelium
  • Way of defence against acid
  • Commonest in obese men >50
  • Often asymptomatic
  • Premalignant
  • Low grade dysplasia -> high grade dysplasia -> adenocarcinoma
  • Approx. 0.3% p.a (ie 1/300pt year)
  • Surveillance vs. ablation
  • Long-term treatment with PPI
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5
Q

gord complications

A
  • Oesophagitis
  • Peptic stricture (benign narrowing of oesophagus)
  • Barrett’s oesophagus
  • Adenocarcinoma
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6
Q

treatment of GORD

A
  • Lifestyle measures (smoking, alcohol, diet, weight reduction)
  • Mechanical (posture, clothing, elevate bedhead)
  • Antacids
  • Acid suppression
  • Surgical- fundoplication
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7
Q

achalasia

A

MOTILITY DISORDER

  • Failure of LOS relaxation
  • Absence of peristalsis
  • Incidence 1/100.000
  • Degenerative lesions of oesophageal innervation
  • Presents with dysphagia to liquids and solids, weight loss, chest pain
  • Endoscopic appearances usually normal
  • Can progress to oesophageal dilation and respiratory complications
  • Treatment -> BoTox, endoscopic dilation, surgical myotomy, POEM
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8
Q

eosiniphilic oesophagitis

A
  • Common presentation with food bolus obstruction, dysphagia
  • Younger age, M>F
  • Prevalence 50/ 100,000
  • History of atopy (asthma, hay fever)
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9
Q

treatment of eosiniphilic oesophagitis

A
  • Diet – elimination (egg, wheat, milk, nuts, soya, fish)
  • Drugs – PPI, tropical sterols (budesonids, fluticasone)
  • Dilation – for strictures
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10
Q

oesophageal cancer - adenocarcinoma

A
  • Lower third oesophagus
  • Younger
  • Reflux (Barrett’s)
  • Obesity
  • More common
  • Increasing
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11
Q

oesophageal cancer - squamous cell carcinoma

A
  • Mid/ upper oesophagus
  • Older
  • Smoking
  • Alcohol
  • Less common
  • Declining
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12
Q

eosinophilic oesophagitis

- investigations

A
  • Endoscopy – furrows, rings, exudates, strictures
  • Biopsy for diagnosis (>15 eosinophils / pof)

6 Biopsies

  • 3 from upper, 3 from mid
  • If any biopsies there’s more than 15 eosinophils per high-powered field = diagnosis
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13
Q

treatment for H.Pylori

A

First line (90% efficacy)

  • Lansoprazole 30mg 2x a day
  • Clarithromycin 500mg 2x day
  • Metronidazole 400mg 2x a day
  • All 3 for 1 week

Second line if this doesn’t work (85-90% efficacy)
- Another 3 for 1 week

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14
Q

maldigestion

A
  • Impaired breakdown of nutrients, luminal phase (eg pancreatic insufficiency)
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15
Q

malabsorption

A
  • Defective mucosal uptake and transport of adequately digested nutrients. Selective or global
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16
Q

malassimilation

A

maldigestion + malabsorption

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17
Q

luminal phase of absorption affected by…

A

Nutrient hydrolysis
- Enzyme deficiency – pancreatic insufficiency
- Enzyme inactivation – ZE syndrome
- Inadequacy of mixing – rapid transit, surgical resection
Fat Solubilization
- Decreased bile salts – cholestasis, cirrhosis
- Bile salt deconjugation – bacterial overgrowth
- Bile salt loss – ileal disease or resection
Luminal availability
- Bacterial consumption of nutrients (bacterial overgrowth) – B12 deficiency
- Decreased intrinsic factor (pernicious anaemia – B12 deficiency

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18
Q

mucousal phase of absorption is affected by…

A

Brush border hydrolysis
- Lactase deficiency (post gastroenteritis, alcohol, radiation)

Epithelial transport

  • Reduced absorptive surface – resection
  • Damaged absorptive surface – coeliac disease, tropical sprue, Crohn’s disease, ischaemia
  • Infections – Giardia, SIBO
  • Infiltration – lymphoma, amyloid
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19
Q

post-mucousal phase of absorption is affected by…

A
  • Post-absorptive processing – lymphatic obstruction

- Lymphangectasia, neoplastic, TB

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20
Q

clinical features of malabsorption

A
  • Diarrhoea and weight loss despite adequate intake
  • Bloating, distention, cramps, borborygmi
  • Lethargy, malaise
  • Symptoms often mild, non-specific
  • Malabsorption can be global, or specific nutrients
  • Malabsorption syndrome (steatorrhoea, distention, weight loss, oedema) is a RARE presentation
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21
Q

clues of malabsorption in patient history

A
  • Weight loss
  • Diarrhoea/ stearorrhea (bile salts and fat)
  • Abdominal distention/ gas (carbohydrate)
  • Intestinal “angina” (vasculopathy)
  • Metabolic bone disease
  • GI surgery
  • Pancreatitis
  • Cystic fibrosis
  • Alcohol
  • FHx coeliac
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22
Q

clues of malabsorption on examination

A
  • Evidence of malnutrition
  • Skin
  • Angular cheilitis, glossitis
  • Dermatitis herpetiformis
  • Oedema
  • Neurologic (B12)
  • Peripheral neuropathy
  • Ataxia (posterior column)
  • Psychosis, dementia
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23
Q

laboratory clues of malabsorption

A
  • Microcytosis
  • Iron deficiency (common in coeliac, otherwise suspect GI blood loss)
  • Macrocytosis
  • B12, folate deficiency, but also common in coeliac, alcohol
  • Elevated ALP +/- low Ca
  • Hypalbuminaemia
  • Evidence of multiple deficiencies
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24
Q

main 3 causes of malabsorption

A
  • Coeliac disease
  • Pancreatic insufficiency
  • Small bowel overgrowth (SIBO) – bacterial overgrowth
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25
Q

coeliac disease general

A
  • Small bowel disorder characterized by
  • Mucosal inflammation
  • Villous atrophy
  • Crypt hyperplasia
  • Which occur upon exposure to dietary gluten and which demonstrate improvement after withdrawal of gluten from the diet
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26
Q

symptoms of coeliac disease

A
  • Diarrhoea
  • Anaemia
  • Dyspepsia
  • Abd pain, bloating
  • Weight loss
  • Mouth ulcers
  • Fatigue
  • Neuropsychiatric symptoms
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27
Q

clues on investigation - coeliac disease

A
  • Anaemia
  • Iron, folate deficiency
  • Macrocytosis without anaemia
  • Hyposplenic blood film
  • Low calcium, elevated alk phos
  • Raised transaminases
  • Hypalbuminaemia
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28
Q

diagnosis of coeliac disease

A
  • Serological markers
  • Anti-tissue transglutaminase antibody (IgA)
    (TGG) sensitivity and specificity >95%
  • Anti-endomysial antibody (IgA)
  • Anti-gliadin antibody (IgA, IgG)
  • Small intestinal biopsy
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29
Q

treatment for coeliac disease

A
  • Gluten free diet (life-long)
  • Dietician
  • Nutritional supplements
  • Screen for complications
  • Bone disease
  • Very rarely, need for immunosuppressant medication for refractory cases
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30
Q

pancreatic exocrine insufficiency (PEI)

A
  • Pancreas produces 1.5L/day of bicarbonate and enzyme-rich fluid
  • Enzymes for digestion of fat, protein, CHO
  • Lipolytic activity declines at first so fat absorption mainly affected
  • Overt clinical consequences unlikely unless 90% function loss
  • Steatorrhea, weight loss, vit. Deficiency (A, D, E, K) also more minor symptoms
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31
Q

causes of PEI

A
  • Chronic pancreatitis (alcohol)
  • Pancreatic cancer
  • Cystic fibrosis
  • Haemochromatosis
  • Pancreatic resection
  • Gastric resection
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32
Q

PEI diagnosis

A
  • Risk factors (alcohol, CF)
  • Symptoms
  • Pancreatic imaging (CT, MRI)
  • Tests of exocrine pancreatic function
  • Direct – eg secretin stimulation tests
  • Indirect – eg faecal elastase, pancreolauryl (only reliably detect mod. To severe PEI)
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33
Q

PEI treatment

A
  • Pancreatic enzyme replacement
  • Taken with meals and snacks
  • Gastric acid suppression
  • Vitamin supplements
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34
Q

small intestinal bacterial overgrowth (SIBO)

A
  • Normally 10^5 to 10^9 bacteria/ml present in distal small bowel
  • Colon has up to 10^12
  • Older patients, immunosuppressed, disturbed function/ anatomy of gut
  • Mostly gram- aerobic bacteria in ileum, gram+ anaerobic bacteria in colon
  • In bacterial overgrowth this balance is lost
  • Bacteria moves up to s. intestine
  • Competes for food
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35
Q

causes of SIBO

A
  • Stasis (stop in flow of gut)
  • Strictures
  • Crohn’s disease
  • TB
  • Hypomobility
  • Old age
  • Opiate analgesics
  • Diabetes
  • Systemic sclerosis

Blind loops, diverticulae

  • Used to be common, now more common again
  • Bacteria less likely to be flushed through
  • As a result of gastric surgery for peptic ulcer disease
  • Now patients with obesity having surgery
  • Immunodeficiency
  • Obesity?
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36
Q

diagnosis of SIBO

A
  • Quantative culture of jejunal fluid is gold standard
  • Glucose/ hydrogen breath test
  • More practical
  • Oversenstive
  • Small bowel radiology to look for anatomical abnormalities
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37
Q

SIBO treatment

A
  • Treatment with 2 weeks of antibiotics
  • Eg tetracycline, ciprofloxacin, rifaximin
  • Often needs repeat treatments
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38
Q

bile acid malabsorption (BAM)

A
  • Bile acids specifically absorbed in ileum
  • Cause secretory diarrhoea in colon
  • Affected by ileal disease or resection
  • Also impaired in post-cholecystectomy, rapid transit and other malabsorptive states
  • Primary BAM may reflect over-production rather then malabsorption
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39
Q

Giarda lamblia

A
  • Non-invasive pathogen
  • Malabsorption due to multiple factors
  • Brush border damage
  • Reductions in surface area
  • Bile acid utilization
  • Induction of hypermotility
  • Enterotoxin
  • Treatment of choice is metronidazole
40
Q

what types of polyps are cancerous or not

A
  • Not all colonic polyps progress to adenocarcinoma
  • Adenomas have the highest progression potential to adenocarcinomas
  • Hyperplastic (metaplastic polyps don’t have malignant potential)
  • A special type of hyperplastic polyp called serrated polyp has some malignant potential
41
Q

risk factors for colorectal cancer

A
  • diet high in red meats and processed meats
  • cooking meat at vv high temp - cretes chemicals
  • diet low in fibre
  • obesity
  • physical inactivity
  • smoking
  • alcohol excess
  • family history of colorectal polyps or colorectal cancer
  • a family history of colorectal polyps or colorectal cancer
  • history of IBS
  • older age
42
Q

what nerve innervates the oesophagus

A

Oesophagus innervated by vagus nerve and sympathetic fibres

- Branch of vagus -> left recurrent laryngeal nerve

43
Q

oesophageal constrictions

A

Superiorly

  • Level of cricoid cartilage
  • At juncture of pharynx

Middle

  • Crossed by aorta
  • Left main bronchos

inferior
- diaphragmatic sphincter

44
Q

oesophageal histology

A

mucosa

  • starified squamous
  • non keratinizing
  • muscularis mucosa

submucosa
- mucous glands

muscularis externa

adventitia

  • loose conn. Tissue
  • no serosa
45
Q

cancer staging T in the oesophagus

A

any tumour that invades 3 layers (mucosa, submucosa, muscularis mucosa)
- considered T1

once tumour goes to muscularis propria
- T2

Once touches adventitia/serosa of oesophagus
- T3

Once tumour out of layers of oesophagus and into nearby organs
- T4

46
Q

symptoms of oesophageal tumour

A
  • Dysphagia of solids (and liquids when worse)
  • Feeling of food getting stuck / choking
  • Hoarse voice
  • Weight loss
47
Q

superior mesenteric vein

A

Draws blood from small bowel and right side of large bowel

48
Q

inferior mesenteric vein

A

Draws blood from left side of large bowel

Joined by splenic vein that gets blood from vein

49
Q

left gastric vein

A

Take blood from lesser curve of stomach and branches from fondus of stomach

50
Q

what 3 structures make up the portal vein

A

superior mesenteric vein
inferior mesenteric vein
splenic vein

51
Q

coronary vein

A

Brings blood from portal vein into the peri oesophageal plexus

Lower end of oesophagus drains from this vein into the portal system

52
Q

liver cirrhosis

A
  • Liver becomes nodular and stiff
  • Blood from portal vein can’t get through the liver easily
  • Inc. pressure in portal systems

Flow of blood slows down

  • Leading to collateral circulation
  • Shunting of blood = reversal of flow of blood down to the portal vein from the liver
  • Blood from portal vein goes into the peri oesophageal plexus and forms ESOPHAGEAL VARICES
  • Collaterals drain into hemi-azygos and azygos systems
  • Eventually blood goes into the superior vena cava and returns into the systemic circulation
53
Q

if pressures are really high in liver cirrhosis

A
  • Then there’s reversal of flow of the splenic vein
  • Blood can no longer be drained from spleen down to the portal vein

Collateral circulation forms that joins in fundus of stomach – peri oesophageal plexus

  • GASTRIC VARICES
  • Through this system blood finds its way back into systemic circulation
54
Q

what happens if there’s clots in the splenic vein

A
  • Eg in acute pancreatitis
  • Then blood no longer drains from the spleen

Has to create collaterals

  • So drains through the fundus of stomach
  • Gastric varices

Called SEGMENTAL PORTAL HYPERTENSION

55
Q

clots in superior mesenteric vein territory

A
  • Due to lots of inflammation in the area of the small bowel
  • Eg bowel ischaemia or trauma
  • Regional formation of collaterals
  • Forms varices in small bowel
  • Blood may bypass this area creating anastomoses with nearby vessels
56
Q

treatment of varices

A
  • Endoscope goes down
  • Suction
  • Place bands
  • Thombose/ clot areas
  • Trying to divert blood flow from superficial layers of oesophagus to deeper layer
57
Q

treatment of gastric varices

A

Banding gastric varices is harder because they’re bigger

  • Risk that band falls off and there’s a hole left
  • Could lead to life threatening bleeding

So treatment of gastric varices is…

  • Inject thrombotic agent such as thrombin into the varix
  • Varix will swell due to thrombosis
58
Q

regions of the stomach

A
  • Cardiac
  • Fundus (where gastric varices form)
  • Corpus
  • Pyloric -> antrum, pyloric canal, sphincter
59
Q

stomach histology

A
  • Glands in all zones have mucous cells and enteroendocrine cells

Fundic glands

  • Parietal (oxyntic cells) cells – HCI, intrinsic factor
  • Chief (zymogenic) cells – pepsinogen, rennin, lipases
  • Mucous neck cells
  • Enteroendocrine cells gastrin, cholecystokinin, secretin, serotonin, glucagon
60
Q

coeliac axis contains…

A

the Coeliac trunk is in the abdominal aorta it contains…

Left gastric artery

Common hepatic artery

  • Right gastric
  • Proper hepatic artery
  • Right, left and middle
  • 2 branches that go to duodenum
  • Supra duodenal artery
  • Gastro duodenal artery

Splenic artery

61
Q

what does the left gastric artery supply

A

upper part of stomach and lesser curve

62
Q

what does the right gastric artery supply

A

supplies stomach

63
Q

what does the splenic artery supply

A

goes behind stomach and supplies blood to the spleen, pancreas and stomach

64
Q

what does the gastro-duodenal artery supply and what about this is significant

A

supplies blood to duodenal bulb and the posterior aspect of the duodenum

  • Post. Aspect of duodenum is often area of duodenal ulcers
  • Gastro duodenal artery can be invaded by ulcers
  • Causing significant bleeding
65
Q

lymph nodes in the coeliac axis

A
  • With gastric cancer coeliac axis area often affected
  • Important area in staging of cancer
  • If coeliac access is affected in oesophageal cancer it’s considered as metastasis
66
Q

gallstones

A
  • Form in gall bladder
  • If stone leave gall bladder and goes down bile duct
  • Cause obstruction
  • Bile no longer flows down
  • Bile Spills over into blood
  • Patients can develop jaundice
67
Q

what does a tumour at the head of the pancreas present with

A
  • Stops the flow of bile down into the duodenum
  • Gall bladder becomes enlarged
  • Unlike with gallstones it’s not painfuL
  • If there’s a mass the duct dilates – gall bladder big
  • So jaundice but painless
  • Present with weight loss and back pain]
68
Q

what arteries supply the fore, mid and hind gut

A
  • Coeliac trunk = foregut
  • Superior mesenteric = mid gut (small intestine, right of large intestine)
  • Inferior mesenteric = hind gut (left side of large bowel, descending colon, sigmoid, rectum)
    Transverse colon supplied by sup. and inf. Depending on anatomy
69
Q

what does narrowing of the superior mesenteric artery lead to

A
  • Leads to ischaemia in small intestine
  • Called ABDOMINAL ANGINA
  • Patients complain of abdominal pain after eating
  • Bc after eating lots of blood has to go into intestines for digestion
  • So when that can’t happen = pain
70
Q

causes of mucosal injury in the GI tract

A
Gi secretions
ischaemia
drugs
immunological
infections
radiation
trauma
idiopathic
71
Q

manifestations of mucosal injury

A
  • Inflammation
  • Apoptosis or necrosis
  • Erosion and ulceration
  • Hypoplasia and atrophy
  • Metaplasia
  • Dysplasia +/- neoplasia
72
Q

acute gastritis

A
  • Acute erosive / haemorrhagic gastritis
    Ingestion of irritant
    chemicals
  • Acute H. pylori infection
    Usually no minor symptoms, so seldom seen in biopsies
73
Q

chronic gastritis

A
  • Non-atrophic gastritis
  • Chronic H. pylori infection
  • Atrophic gastritis
  • Autoimmune gastritis
  • Antibodies made against parietal cells
  • Loss of intrinsic factor secretion (B12)
  • Leads to anaemia
  • Chronic H. pylori infection
74
Q

chronic gastritis - special forms

A
  • Chemical gastritis
  • Eg bile reflux, NSAIDs
  • Radiation gastritis
  • Lymphocytic gastritis
  • Associated with coeliac disease
  • Non-infectious granulomatous gastritis
  • Eg crohn’s disease, sarcoidosis
  • Eosinophilic gastritis
  • Eg food sensitivities
  • Other infectious gastritides (non-H. pylori)
  • Bacteria viruses (eg CMV) fungi, parasites
75
Q

what is coeliac disease

A
  • Hypersensitivity to glutamine-rich proteins in wheat, barley and rye
  • Strong link to certain HLA class II genes
  • Leads to malabsorption due to injury to mucosa of small intestine
76
Q

how do you diagnose coeliac disease

A
  • Typical histological changes from biopsy of small intestine (duodenum)
  • Autoantibodies in the blood
  • Improvement of symptoms after gluten-free diet
  • Often picked up in screening for iron deficiency
77
Q

what skin condition is related to coeliac disease

A

dermatitis herpetiforms

78
Q

histological features of coeliac disease

A
  • Loss of villus architecture
  • Chronic inflammation in the lamina propria
  • Increased no. of T lymphocytes in epithelium
  • Epithelial damage
  • Crypt hyperplasia
79
Q

what is the genetic component of IBD

A
  • Having a family member with IBD is the biggest RF
  • Monozygotic twin studies have shown greater concordance for crohns disease than UC
  • Various susceptibility genes identified
  • NOD2 gene in crohn’s disease (involved in bacterial recognition)
80
Q

what is the purpose of biopsy in IBD

A
  • Exclude other aetiologies eg infection
  • Make initial diagnois of IBD
  • Distinguish between UC and Crohns
  • Assess response to treatment
  • Look for complications or other pathology
  • Surveillance for dysplasia
81
Q

epithelial pathological changes in IBD

A
  • Epithelial damage/ erosion/ ulceration
  • Mucin depletion
  • Neutrophil infiltration (“cryptitis’ and crypt abscesses)
  • Metaplasia
82
Q

lamina propria inflammatory cell infiltrate in IBD

A
  • Cell types (plasma cells, neutrophils etc)
  • Density of inflammatory infiltrate
  • Distribution of infiltrate (patchy vs. diffuse)
  • Presence of granulomas
83
Q

general architecture changes in IBD

A
  • Surface topography

- Crypt architectural abnormalities/ atrophy

84
Q

ulcerative colitis general info

A
  • Chronic relapsing and remitting clinical course
  • Recurrent episodes of rectal bleeding
  • Highest incidence 15-25, smaller in 60-70 yrs
  • No gender diff
  • Inflammation confined to mucosa unless severe
  • Typically involves rectum +/- left colon
  • Involvement of whole colon (pancolitis) is a continuous distribution
85
Q

what are pseudopolyps

A

scar tissue projection from ulceration on bowel wall

86
Q

crohn’s disease

A
  • Regional enteritis
  • Chronic, multifocal, relapsing condition that can affect any part of the GI tract
  • Peak incidence 20-30, smaller peak 60-70
  • No gender diff.
  • Variety of presenting complaints depending on what part of GI tract
  • Abdominal pain, diarrhoea, weight loss, strictures and obstruction, fistulae
  • Transmural inflammation (involves all the layers of the wall)
  • Patchy and discontinuous
87
Q

presence of granulomas in crohns disease

A
  • Presence of granulomas in 70% of cases
  • Due to activated macrophages
  • Fewer in right colon than left
  • More common in children
  • But larger in adults
  • Fewer after 2 years of illness
  • Granulomas can be identified in all layers of wall
  • If in mucosa can be associated with UC
  • So more helpful to diagnose CD is deeper within the wall
  • In lymph nodes**
88
Q

ulceration in crohn’s disease

A
  • Not broad flat ulcers like in UC
  • Aphis ulcers
  • Small, superficial ulcers over mucosa
  • In crohn’s ulceration often extends into the anal canal and involves the peri anal skin
89
Q

fistulas

A
  • If bowel stuck to adjacent organs/ other segments of bowel
  • The fissuring ulceration can give rises to a fistula
  • An abnormal structure between 2 hollow organs or hollow organ and skin surface
90
Q

what features are presnet in CD and not UC

A
  • subacute intestinal obstruction
  • fistulae
  • malabsorption
  • cobblestone patterns of ulcers in Crohns
91
Q

toxic dilation

A
  • Emergency presentation
  • Massively distended large bowel loops
  • Cause damage to nerve supply of the colon
  • Large bowel wall becomes vv thin and perpherates easily
92
Q

neoplasia in IBD

A
  • higher risk for UC
  • risk inc. with time since diagnosis
  • risk inc. with severity and extent of disease
  • most commonly COLORECTAL CARCINOMAS
  • also SMALL BOWEL CARCINOMAS
  • other eg bile duct carcinomas, leukaemia’s
  • about 5% with CD
  • about 11% with UC
93
Q

conditions that mimic IBD

A
  • infective colitis – bacterial and parasitic
  • sexually transmitted looks like UC
  • Ischaemic colitis
  • Most common in region of splenic flexure and descending colon
  • Can look like crohns endoscopically but not histologically
  • Diverticular disease
  • Most common in sigmoid colon
  • Can result in fistulaes to toher organs eg bladder
  • Mimics crohns histologically and radiologically
  • Drug induced colitis
  • NSAID – ileocolic region
  • Radiation colitis
  • Endoscopically resembelance
  • Neoplasia
  • Can give rise to mass lesions, fistulae and strictures
94
Q

causes of colonic strictures

A
  • Crohn’s disease
  • Ischaemic colitis
  • Diverticular disease
  • Diaphragm disease – NSAIDS
  • Neoplasia
95
Q

microscopic colitis

A
  • Usually seen in older patients
  • Chronic watery diarrhoea
  • Over several months
  • Normal appearance of colonic and rectal mucosa at endoscopy
  • Must look at microscopy
  • Inc. in chronic inflammatory cells in lamina propria
  • 2 patterns
  • Collagenous colitis
  • Lymphocytic colitis
  • Cause isn’t identified
  • Lymphocytic colitis can be assoc. with coeliac disease
  • Drugs implicated in some cases, particularly PPI, NSAIDS
  • Can be treated with steroids