wk 3/4 GI Flashcards
GORD symptoms
- acid reflux
- heart burn
- waterbrash
- often meal related
- postural (when lying down)
investigations of oesophageal disease
- endoscopy or biopsy
- barium swallow test
- oesophageal function test (manometry, pH & impendence monitoring)
reflux oesophagitis
- 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
barrett’s oesophagus
- 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
gord complications
- Oesophagitis
- Peptic stricture (benign narrowing of oesophagus)
- Barrett’s oesophagus
- Adenocarcinoma
treatment of GORD
- Lifestyle measures (smoking, alcohol, diet, weight reduction)
- Mechanical (posture, clothing, elevate bedhead)
- Antacids
- Acid suppression
- Surgical- fundoplication
achalasia
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
eosiniphilic oesophagitis
- Common presentation with food bolus obstruction, dysphagia
- Younger age, M>F
- Prevalence 50/ 100,000
- History of atopy (asthma, hay fever)
treatment of eosiniphilic oesophagitis
- Diet – elimination (egg, wheat, milk, nuts, soya, fish)
- Drugs – PPI, tropical sterols (budesonids, fluticasone)
- Dilation – for strictures
oesophageal cancer - adenocarcinoma
- Lower third oesophagus
- Younger
- Reflux (Barrett’s)
- Obesity
- More common
- Increasing
oesophageal cancer - squamous cell carcinoma
- Mid/ upper oesophagus
- Older
- Smoking
- Alcohol
- Less common
- Declining
eosinophilic oesophagitis
- investigations
- 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
treatment for H.Pylori
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
maldigestion
- Impaired breakdown of nutrients, luminal phase (eg pancreatic insufficiency)
malabsorption
- Defective mucosal uptake and transport of adequately digested nutrients. Selective or global
malassimilation
maldigestion + malabsorption
luminal phase of absorption affected by…
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
mucousal phase of absorption is affected by…
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
post-mucousal phase of absorption is affected by…
- Post-absorptive processing – lymphatic obstruction
- Lymphangectasia, neoplastic, TB
clinical features of malabsorption
- 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
clues of malabsorption in patient history
- 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
clues of malabsorption on examination
- Evidence of malnutrition
- Skin
- Angular cheilitis, glossitis
- Dermatitis herpetiformis
- Oedema
- Neurologic (B12)
- Peripheral neuropathy
- Ataxia (posterior column)
- Psychosis, dementia
laboratory clues of malabsorption
- 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
main 3 causes of malabsorption
- Coeliac disease
- Pancreatic insufficiency
- Small bowel overgrowth (SIBO) – bacterial overgrowth
coeliac disease general
- 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
symptoms of coeliac disease
- Diarrhoea
- Anaemia
- Dyspepsia
- Abd pain, bloating
- Weight loss
- Mouth ulcers
- Fatigue
- Neuropsychiatric symptoms
clues on investigation - coeliac disease
- Anaemia
- Iron, folate deficiency
- Macrocytosis without anaemia
- Hyposplenic blood film
- Low calcium, elevated alk phos
- Raised transaminases
- Hypalbuminaemia
diagnosis of coeliac disease
- Serological markers
- Anti-tissue transglutaminase antibody (IgA)
(TGG) sensitivity and specificity >95% - Anti-endomysial antibody (IgA)
- Anti-gliadin antibody (IgA, IgG)
- Small intestinal biopsy
treatment for coeliac disease
- Gluten free diet (life-long)
- Dietician
- Nutritional supplements
- Screen for complications
- Bone disease
- Very rarely, need for immunosuppressant medication for refractory cases
pancreatic exocrine insufficiency (PEI)
- 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
causes of PEI
- Chronic pancreatitis (alcohol)
- Pancreatic cancer
- Cystic fibrosis
- Haemochromatosis
- Pancreatic resection
- Gastric resection
PEI diagnosis
- 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)
PEI treatment
- Pancreatic enzyme replacement
- Taken with meals and snacks
- Gastric acid suppression
- Vitamin supplements
small intestinal bacterial overgrowth (SIBO)
- 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
causes of SIBO
- 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?
diagnosis of SIBO
- Quantative culture of jejunal fluid is gold standard
- Glucose/ hydrogen breath test
- More practical
- Oversenstive
- Small bowel radiology to look for anatomical abnormalities
SIBO treatment
- Treatment with 2 weeks of antibiotics
- Eg tetracycline, ciprofloxacin, rifaximin
- Often needs repeat treatments
bile acid malabsorption (BAM)
- 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
Giarda lamblia
- 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
what types of polyps are cancerous or not
- 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
risk factors for colorectal cancer
- 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
what nerve innervates the oesophagus
Oesophagus innervated by vagus nerve and sympathetic fibres
- Branch of vagus -> left recurrent laryngeal nerve
oesophageal constrictions
Superiorly
- Level of cricoid cartilage
- At juncture of pharynx
Middle
- Crossed by aorta
- Left main bronchos
inferior
- diaphragmatic sphincter
oesophageal histology
mucosa
- starified squamous
- non keratinizing
- muscularis mucosa
submucosa
- mucous glands
muscularis externa
adventitia
- loose conn. Tissue
- no serosa
cancer staging T in the oesophagus
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
symptoms of oesophageal tumour
- Dysphagia of solids (and liquids when worse)
- Feeling of food getting stuck / choking
- Hoarse voice
- Weight loss
superior mesenteric vein
Draws blood from small bowel and right side of large bowel
inferior mesenteric vein
Draws blood from left side of large bowel
Joined by splenic vein that gets blood from vein
left gastric vein
Take blood from lesser curve of stomach and branches from fondus of stomach
what 3 structures make up the portal vein
superior mesenteric vein
inferior mesenteric vein
splenic vein
coronary vein
Brings blood from portal vein into the peri oesophageal plexus
Lower end of oesophagus drains from this vein into the portal system
liver cirrhosis
- 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
if pressures are really high in liver cirrhosis
- 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
what happens if there’s clots in the splenic vein
- 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
clots in superior mesenteric vein territory
- 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
treatment of varices
- Endoscope goes down
- Suction
- Place bands
- Thombose/ clot areas
- Trying to divert blood flow from superficial layers of oesophagus to deeper layer
treatment of gastric varices
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
regions of the stomach
- Cardiac
- Fundus (where gastric varices form)
- Corpus
- Pyloric -> antrum, pyloric canal, sphincter
stomach histology
- 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
coeliac axis contains…
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
what does the left gastric artery supply
upper part of stomach and lesser curve
what does the right gastric artery supply
supplies stomach
what does the splenic artery supply
goes behind stomach and supplies blood to the spleen, pancreas and stomach
what does the gastro-duodenal artery supply and what about this is significant
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
lymph nodes in the coeliac axis
- 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
gallstones
- 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
what does a tumour at the head of the pancreas present with
- 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]
what arteries supply the fore, mid and hind gut
- 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
what does narrowing of the superior mesenteric artery lead to
- 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
causes of mucosal injury in the GI tract
Gi secretions ischaemia drugs immunological infections radiation trauma idiopathic
manifestations of mucosal injury
- Inflammation
- Apoptosis or necrosis
- Erosion and ulceration
- Hypoplasia and atrophy
- Metaplasia
- Dysplasia +/- neoplasia
acute gastritis
- Acute erosive / haemorrhagic gastritis
Ingestion of irritant
chemicals - Acute H. pylori infection
Usually no minor symptoms, so seldom seen in biopsies
chronic gastritis
- 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
chronic gastritis - special forms
- 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
what is coeliac disease
- 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
how do you diagnose coeliac disease
- 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
what skin condition is related to coeliac disease
dermatitis herpetiforms
histological features of coeliac disease
- Loss of villus architecture
- Chronic inflammation in the lamina propria
- Increased no. of T lymphocytes in epithelium
- Epithelial damage
- Crypt hyperplasia
what is the genetic component of IBD
- 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)
what is the purpose of biopsy in IBD
- 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
epithelial pathological changes in IBD
- Epithelial damage/ erosion/ ulceration
- Mucin depletion
- Neutrophil infiltration (“cryptitis’ and crypt abscesses)
- Metaplasia
lamina propria inflammatory cell infiltrate in IBD
- Cell types (plasma cells, neutrophils etc)
- Density of inflammatory infiltrate
- Distribution of infiltrate (patchy vs. diffuse)
- Presence of granulomas
general architecture changes in IBD
- Surface topography
- Crypt architectural abnormalities/ atrophy
ulcerative colitis general info
- 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
what are pseudopolyps
scar tissue projection from ulceration on bowel wall
crohn’s disease
- 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
presence of granulomas in crohns disease
- 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**
ulceration in crohn’s disease
- 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
fistulas
- 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
what features are presnet in CD and not UC
- subacute intestinal obstruction
- fistulae
- malabsorption
- cobblestone patterns of ulcers in Crohns
toxic dilation
- Emergency presentation
- Massively distended large bowel loops
- Cause damage to nerve supply of the colon
- Large bowel wall becomes vv thin and perpherates easily
neoplasia in IBD
- 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
conditions that mimic IBD
- 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
causes of colonic strictures
- Crohn’s disease
- Ischaemic colitis
- Diverticular disease
- Diaphragm disease – NSAIDS
- Neoplasia
microscopic colitis
- 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
