GI top tier Flashcards
IBD conditions=
- what are they both in general terms
crohn’s
ulcerative colitis
chronic, inflammatory conditions - inappropriate immune responses against gut flora
ulcerative colitis
- age
- gender
- race
20-40
m>f
more prevalent in western populations than general world
risk factors for crohns and UC
Crohn’s
- Smoking damages
UC
- Smoking protects so if smoking – decreases the severity of symptoms
- Some link to HLAB27 (as with ankylosing spondylitis - but less strong of a link)
- Primary sclerosing cholangitis
crohn’s vs UC: distrubtuion
crohns
= Can be anywhere along gut, from mouth to anus
- Most common in terminal ileum - where bile salts and B12 are absorbed
UC
= Starts at the rectum and progresses up.
- Up to colon- can’t go into the ileum past the ileocaecal valve.
- (backwash ileitis = reflux back into ileum but not intrinsically inflamed ileum)
- Classified by how much of colon is affected
crohns vs UC pattern of inflammation
how do inflamed areas appear?
crohns
=Patchy inflammation, not continuous (has skip lesions)
UC
=Continuous inflammation, not patchy. Distinct cut off between normal and inflamed regions:
- Inflamed = ulcerated and darker (hyperaemic = red in colonoscope but more brown in resections)
crohn’s vs UC bowel wall affected how
crohn’s =The full thickness of the bowel wall can be affected (can be transmural) - mucosa, submucosa, muscularis propria, fat
UC=Only the mucosal layer can be affected
crohns vs UC ulcers
what about fistula?
crohns= Deep fissuring ulcers
UC = ulcers also present
chrons = Yes (deep fistula go through to other bits of bowel) UC = no
crohns’ vs UC granulomas
+ what is a granuloma
granuloma = collection of epithelial macrophages surrounded by lymphocytes
crohns = yes UC= no
crohn’s vs UC effect on gut cells / features / looks like
crohns = cobblestone mucosa - as a result of fibrosis and strictures
UC =
goblet cell depletion
crypt abscesses and distortion
crohns vs UC- style of chronic disease
both = remission and relapse
signs/ symptoms of IBD (C+UC)
only crohns presentation
BOTH
- Finger clubbing
- Maybe mouth ulcers
- Abdominal tenderness
- Spondylarthropathies
- Diarrhea, sometimes bloody – bowel urgency. Nocturnal diarrhea YES ( not in IBS)
- Abdominal pain, cramps
- Weight loss/failure to thrive/anorexia
- Fatigue, fever, malaise, anorexia, tachycardia
- and complications
CROHNS
- Perianal abscess /fistulae/ skin tags (See complications)
- Malnutrition effects
IBD investigations
Stool sample
- Exclude pathogenic cause
- Faecal calprotectin is present → highly sensitive, indicates GI inflammation
Colonoscopy / sigmoidoscopy / rectal biopsy
- Biopsy taken- Histology
Capsule endoscopy= capsule swallowed and takes pictures as it travels – useful for small bowel
AXR
- No faecal shadows
- Mucosal thickening in UC
- Free air if perforated
Barium x ray
- UC =Lead pipe colon on barium x ray
- Crohns =String sign on barium x ray
Bloods -
- may show elevated wbc
- esr/crp raised with inflammation
- LFTs- UC has strong link with primary sclerosing cholangitis)
- Blood culture - rule out other things
- pANCA in UC (and PSC)
crohns non-surgical treatment
- Questran—Causes bile salts to be absorbed more in the terminal ileum so can be reused by the liver. It also means there are less in the large bowel so more water is reabsorbed into colon and less diarrhea.
- Quit smoking
- Diet- enteral = liquid
- Prednisolone- then taper it off (induces but doesnt maintain remission - may relapse)
- Thiopurine - maintain remission (Azathioprine )
- If severe: IV fluid and IV steroids. Consider blood transfusion
- Biologics
- – Anti TNF (infliximab)
- – Anti IL 12/ 23 (ustekinumab)
- – Anti integrin (targets adhesion molecules)
UC non surgical treatment
- Mesalazine - 5-aminosalicylic acid (for mild) - Not for crohns
- Prednisolone (for moderate)
- IV fluids, IV steroids (for severe)
surgery for IBD
- for each
Resection!
- For UC:
- – removal is curative!!!
- – I think do if medication isn’t working
- For crohns:
- – When a stricture forms
- – Perforation
- – Fistulae
- – Abscess
- – Drugs arent working adequately
crohns complications
Bowel mainly
- Malabsorption
— If sections are resected /mucosal damage is extensive in the small bowel
- Obstruction
— Due to acute swelling, or chronic fibrosis → obstruction and dilatation
- Perforation -Of the deep fissuring ulcers → acute abdomen
- Fistula formation
When deep ulcers go through to other bits of bowel
- Anal skin tags
— Most skin tags checked for crohn’s at histopathology (but most are neg)
- Anal fissures and fistulas
— fissure= dead end, fistula = tunnel
- Neoplasia : Increase in risk of colorectal cancer. Worse if uncontrolled crohns. UC risk is worse
Non bowel = systemic
- Amyloidosis = deposition of beta pleated sheet proteins (rare)
amyloidosis =
deposition of beta pleated sheet proteins (systemic)
UC complications
Colon - due to inflammation
- Ulceration → blood loss
- Toxic dilatation (really swollen)- can rupture → peritonitis
- Colorectal cancer (rare), worse if uncontrolled UC
Larger increase in risk than crohns
Joints
- Ankylosing spondylitis (spine joints fused, bamboo spine)
- Arthritis
Eyes
- Iritis
- Uveitis
- Episcleritis
Skin
- Erythema nodosum = red nodules
- Pyoderma gangrenosum (ulcer wounds)
Liver
- Sclerosing cholangitis
- Fibrosis of bile ducts → obstruct bile flow
- Chronic pericholangitis
- Fatty change
IBS
- age
- gender
- commonnes
- risk factors
- Age onset less than 40
- F >m
- Very common in westerm world
- anxiety,
- previous severe/ long diarrhea
IBS causes -5
what exacerbates it -4
Unknown organic cause (this absence is key)
Causes
- Depression
- Anxiety
- stress/ trauma (Sexual, physical/ verbal abuse)
- GI infection
- Eating disorders
Symptoms exacerbated by
- Stress
- Gastroenteritis
- menstruation
- food
IBS ! - differences from IBD
INVESTIGATION
- normal investigation results
PRESENTATION
- no fever
- no symptoms outside GI tract
- no blood in stool inc meleana (dark/black poo - blood higher in tract)
- no weight loss
- bloating present
- no mouth ulcers
- more constipation
- no nocturnal diarrhea
IBS! - similarities to IBD
- persistant / fluctuating symptoms
- food triggers
- excarbated by stress
IBS
- term describes what?
- chornic/ acute
- types
IBS = group of symptoms, Without any evidence of underlying cause
chronic
4 groups
IBS-D : diarrhea common
IBS-C : constipation common
IBS-M : both diarrhea and constipation common
IBS-U: neither diarrhea and constipation common
IBS symptoms
A- Abdominal pain
Relieved by defecation
(Pain 1 day/week for last 3 months (symptoms started 6 months ago - chronic))
B- bloating
C -Change in bowel habit
- often Increased frequency/ loose stool
- Also can be constipation
- No blood
- NO NOCTURNAL DIARRHEA
- Painful period
- Back pain
- Fatigue
- Urinary frequency/ urgency/ nocturia/ incomplete bladder emptying
IBS investigation
No diagnosis - no objective evidence - histology is useless - Rome IV criteria = Recurrent abdominal pain 1 day/week for last 3 months (symptoms started 6 months ago) \+ 2 of - Pain relieved with defecation - Stool frequency change - Stool appearance change
Instead just rule out things
- Aneamia (FBC)
- Inflammation (ESR/CRP)
- Coeliac (tTG antibodies/ alpha gliadin / EMA antibodies)
- Faecal calprotectin (IBD)
IBS management
- Education
- Reassurance
Dietary modification
- Low FODMAP = carbs which are poorly absorbed
- Lots of fluids
- Small, regular meals
- Reduce caffeine, alcohol, fizzy drinks
- Less insoluble fibre and fruit if bloating/ IBS-Dv(not dissolved, passes through gut unchanged, bulks up faeces and increases gut motility)
- Fibre good for IBS-C (softens stool, slows down sugar release)
- Low sugar
- Pain treatment
- Psychological
- Laxatives vs antimotility agents (loperamide aka imodium) depending on IBS-C or IBS-D respectively
name the 5 broad causes of malabsorption
1 defective intraluminal digestion 2 insufficient absorptive area 3 lack of digestive enzymes 4 defective epithelial transport 5 lymphatic obstruction
defective intraluminal digestion - causes of malabsorption
Pancreatic insufficiency
- Pancreas produces the majority of digestive enzymes - amylases, proteases, lipases. Lack of these in the intestines → lack of digestion
- Pancreatitis : causes damage to most of the glandular pancreas meaning less or no enzymes are released
- Cystic fibrosis : results in the blockage of the pancreatic duct due to excess mucous meaning enzymes aren’t excreted
Defective bile secretion
- → Lack of fat solubilisation so cannot be absorbed
- Biliary obstruction eg gallstone
- Ileal resection - terminal ileum is where we absorb bile salts so reuptake decreased (eg Crohn’s)
Bacterial overgrowth
- Inhibits intraluminal digestion
- Bugs eat the nutrients
insufficent absorptive area cause of malabsorption
= Microvilli damaged, so surface area decreased, so less absorption potential
Coeliac (gluten sensitive enteropathy)
- Villi short if even present (villous atrophy, crypt hyperplasia), due to allergic reaction to gliadin in gluten
Crohns
- Causes inflammatory damage and then scarring to the lining of the bowel, particularly in the terminal ileum, resulting in cobblestone mucosa → SA for absorption decreased
Giardia lamblia (extensive surface parasitisation)
- Extensive surface of villi and microvilli covered by parasite so food can’t be absorbed
- Cleared with antibiotics
Surgery
- resection/ bypass of small intestine removes surface area
- Procedure for
- – Morbid obesity (less so now - weight loss good but malabsorption aspect is bad)
- – Crohns
- – Infarcted small bowel (atherosclerosis)
coeliac pathophysiology
Gliadin protein from gluten - absorbed into intestine. Processed by transglutaminase (TG) and then presented to an APC Th cell. This causes an allergic reaction to gliadin
→ toxic T cells → intestinal epithelium damage → villous atrophy
villous atrophy and crypt hyperplasia are typical signs - villi short if present
inflamed mucosa
increased epithelial lymphocytes due to autoantibodies created and inflammatory response
lack of digestive enzyme causes of malabsorption
Disaccharide deficiency = lactose intolerance
- lactase enzyme deficient so Lactose in milk can not be broken down/ absorbed
- Undigested lactose passes to colon where bacteria eat –> overgrowth
- they damage brush border
Disaccharide deficiency =
- process
- explanation of symptoms
- commonness
= lactose intolerance
- Lactose in milk can not be broken down so can not be absorbed as lactase enzyme is deficient
- Undigested lactose passes to colon.
- Bacteria in colon eat this, releasing CO2, causing wind and diarrhea
- Bacteria overgrowth as a result too → damages brush border
- Very common, and distribution varies - 80% china, 10% UK (ish!!!)
defective epithelial transport causes of malapbsorption
how common are these?
- Abetalipoproteinemia - lack of specific transporter protein to transport lipoprotein across so particular nutrient not absorbed
- Primary bile acid malabsorption - due to mutation in bile acid transporter protein
- Rare
lymphatic obstruction cause of malabsorption including examples
This is the route that absorbed nutrients go: lymphatics → thoracic duct → inferior vena cava → blood
Lymphoma
TB
what is the differential diagnosis of malabsorption
Insufficient intake – Not malabsorption (would absorb correctly if they were taken in)
general presentation of patient with malabsorption
- anaemic
- Weight loss - despite normal calorie intake
- Abnormal faeces
- – High fat in stool as fat not absorbed
- – Pale
- – Floating
coeliac - which part of the bowel is predominantly affected
what malabsorption disorders may result
proximal bowel
B12, iron, folate, vitamin D, calcium
bile salts aren’t absorbed so maybe prob with fat too
coeliac disease
- gender
- age
- commonness
- Common - over 1% in Europe. Prevalence increasing worldwide
- Normally diagnosed middle-aged, or as a child
- m=f
coeliac risk factors
genetics
- Expressing HLA DQ2/8 (mainly the 2 one)- lots have this antigen but no coeliac but it is needed for disease
- First degree relative of coeliac sufferer
Other autoimmune disorders
- igA deficiency
environmental
- Breast feeding
- Rotavirus in infancy
- gluten (gliadins) trigger
coeliac symptoms
- classic
- non-classic
- are many asymptomatic? how could we catch these
Classic (but not necessarily more common)
- Diarrhea
- Steatorrhea
- Weight loss
- Failure to thrive
- Abdominal pain
- Bloating
Non-classic (but not uncommon)
- IB symptoms
- Iron deficiency anaemia
- Osteoporosis
- Dermatitis herpetiformis
- – Chronic autoimmune skin blistering
- – Itchy blisters, red, clusters
- – Cutaneous manifestation of coeliac
- – Diagnosis = skin biopsy to see IgA deposits
- Chronic fatigue
- Ataxia
- Amenorrhea
- Infertility
- Peripheral neuropathy
- Hyposplenism
- Angular stomatitis = inflammation in one/both corners of mouth
- *associated autoimmune disorders
about ⅓ are silent
- Look at 1st degree relatives of patients
- – Serological screening
- Test if associated disease including autoimmune
coeliac investigation
Serology
- IgA transglutaminase (tTG) antibody *
- IgA anti-endomysial antibody (EMA)*
- Coeliac antibodies but if someone is IgA deficient, test for IgG *
- Alpha gliadin antibody levels *
- Often (but not diagnostic) low ferritin, B12, Hb *
Upper GI endoscopy AND * duodenal biopsy
Histology
- villous atrophy
- Crypt hyperplasia
- Increase in intraepithelial lymphocytes
need to keep gluten up (6w+) for investigations
marsh score for coeliac
0 - normal mucosa 1 - increased number of intraepithelial lymphocytes 2- proliferation of crypts of lieberkuhn 3 - variable villous atrophy 3a - partial villous atrophy 3b - subtotal villous atrophy 3c - total villous atrophy 4 hypoplasia of the small bowel architecture (not all contain this stage)
coeliac disease management
Gluten free diet
- Symptoms reverse. Some have persistent symptoms (Sometimes due to low adherence) . Symptoms despite 12month strict gluten free diet = “unresponsive”
DEXA scan to monitor risk of osteoporosis
Correction for vitamin deficiencies (eg folate, B12, iron, calcium, vitamin D)
pneumococcal vaccine given due to risk of hyposplenia
complications of coeliac disease
- Lymphoma
- Osteoporosis
- Anaemia
- Micronutrient deficiencies
- Dermatitis herpetiformis
- Hyposplenia - So pneumococcal vaccine given
- Secondary lactose intolerance
- Increased risk of malignancy due to increased cell turnover
- Other autoimmune conditions
- Infertility- see symptoms
appendicitis complications (and how to treat them)
Rupture
- Releases infected tissue and faecal matter into peritoneum → peritonitis (serious)
Appendix mass
- If inflamed appendix becomes covered in omentum to form a mass
- Antibiotics and then surgery to remove appendix
Abscess
- Pus and fluid around appendix
- Antibiotics and drain appendix
appendicitis management
- Appendectomy (lapropscopic) = removal of appendix
- IV anitbiotics pre-op to reduce wound infections
- Drain any abscesses
appendicitis investigations inc exclusions
Blood tests
- Raised CRP/ESR
- Raised wbc - neutrophil esp
Ultrasound
- Inflammed appendix/ appendix mass/ diff diganoses
CT = gold standard
Pregnancy test- to exclude ectopic pregnancy
Urinalysis- to exclude UTI
symptoms and signs of appendiciits
- pain
- – Umbilical region
- – Migrates to R iliac fossa
- – Mcburney’s point
- Anorexia
- naus/vom
- Constipation. Or sometimes diarrhea
- Oedema
- Fever
- Tachycardia
- Tenderness in R iliac fossa with guarding – due to localised peritonitis!!
- Tender mass in R iliac fossa
appendicitis
- age
- commonness
- gender
10-20y
common
m>f
appendicitis causes
- Faecolith = a stone made of faeces, can block appendix lumen
- Lymphoid hyperplasia - block lumen – Especially children/teenagers
- Filarial worms (pinworms) block lumen == most common
- Undigested seeds
appendicitis differential diagnosis
name 3
- Ileitus due to crohns
- Salpingitis (fallopian tube inflammation)
- Ectopic pregnancy
- UTI
- Diverticulitis
- Perforated ulcer
- Food poisoning
appendicitis pathophysiology
- Occurs when lumen of appendix becomes obstructed,
- Appendix continues to produce mucous secretions. These build up and increase appendix pressure
- It gets physically bigger and presses on nerves
- Inflammation - pus accumulates –Serum wbc increase
- Oedema
- Ischaemia
- – Swelling presses on blood vessels nearby and these cuts of the blood supply to appendix → cells die
- – Flora in gut now trapped in appendix, they are able to proliferate resulting in the invasion of gut organisms into the appendix wall
- – This means bacteria can invade the wall
- Necrosis
- Perforation — Wall is dead so is very weak so pressure can burst the wall
complications of peptic ulcers
If ulcer erodes through arterial vessel → big bleed/haemorrhage
- Vomiting up blood
If ulcer erodes past the muscle layer
- → peritonitis
- – gas under diaphragm in erect CXR
- – Acute abdominal pain
- → pancreatitis
peptic ulcer investigations
Endoscopy
- These are benign ulcers (not gastric cancer ulcers)
- Punched out
- No heaped up epithelium at edge
- Sharply demarcated
Breath test - C-urea
- Tests for helicobacter pylori
- Quick and reliable, sensitive + specific
- Can monitor after eradication
- No antibiotics/ PPIs before test
Stool antigen test
- Also detects helicobacter
- No PPIs beforehand
- Increase in inflammatory cells
peptic ulcer symptoms
- Upper abdominal pain – Burning pain- indigestion/heartburn = what patient says feels like
- Nausea
what are peptic ulcers
peptic/gastric ulcer found where
- Duodenal ulcers most commonly found in the duodenal cap (first part)
- 2-3x more common than gastric ulcers. Gastric ulcers most commonly seen on lesser curve of stomach but can be anywhere
what are peptic ulcers
4 causes of peptic ulcer (titles only)
- Peptic ulcers: are ulcers (break in superficial epithelial cells penetrating down to muscularis mucosa) in either stomach, duodenum and lower oesophagus
- Associated with an increase in inflammatory cell
- Results in gastritis
causes
- reduced blood flow
- increased acid in stomach
- bile reflux
- infection
what are the warning signs of GI cancer and how to confirm
ALARMS
- Anaemia
- Loss of weight
- Anorexia
- Recent onset/ progressive symptoms
- Melaena = black stools from blood / haematemesis = vomiting blood
- Swallowing difficulty = dysphagia
biopsy to confirm
normal stomach tissues loooks like?
- acidic stomach
- neutral buffered mucin layer (complete)
- glandular gastric cells
- capillary underneath
reduced blood flow cause of ulcer
- pathophysiology
- signs
- treatment
- Mucosa becomes ischaemic
- Cells unable to produce mucin - layer depletes
- Not protected from acidity of stomach
- Those cells die (under no mucin) –> Microulcers (“curling’s ulcers” ) x lots as capillary exposed to acid
- Bleeding
- Cells either side are damaged
- acute
- tachy
- low BP
- maybe haemodynamic shock due to haemorrhage
- restore blood volume (fluids ) –> more bloody supply to mucosa
- reduce stomach acidity with PPI
increased acid in stomach cause of ulcer
- pathophysiology
- causes of increased acid
- treatment
- more acid so able to overcome mucosal mucin barrier
- cells beneath mucin exposed and damaged by acid
- ulceration as capillary and other gastric cells exposed to acid
- Stress!!
- Helicobacter pylori
- Aspirin/aproxen
- – NSAIDs
PPI - reduce acidity (and antibiotics if helicobacter)
how does aspirin / NSAIDs cause ulceration. and how do we counteract this
- NSAIDs sit on mucosa and releases salicylic acid
- This inhibits prostaglandin synthetase (=COX2 or COX1?)
- So less prostaglandins. Prostaglandins needed for mucous secretion
- Ulceration
- SO.. aspirin can be coated in an enteric coat so that is doesn’t dissolve in acid, sit on mucosa and cause ulceration
bile reflux cause of ulcer
- where
- causes
- Bile is okay in duodenum but not in the stomach. so if it refluxes, it is bad (irritation, inflammation)
Causes
- Spirits (rather than wine/beer). These ‘fix’ the stomach (i think this means like preserve it stiff?) - so food passes out less?
- Partial gastrectomy
- intestine blockage
infection cause of ulcers
- causative organism
- pathophysiology
- how to see
- treatment
helicobacter pylori
- Can live in mucin layer in stomach, after being ingested
1. Helicobacter produce chemicals downwards to the cells → causing acute inflammatory cells to be attracted (neutrophils)
2. These move into the gastric epithelium → release things that damage the mucosal cells so they produce less mucus→ ulceration
3. G cells increase acid secretion from parietal cells –> stomach more acidic –> ulceration
4. also causes decrease in duodenal HCO3- secretion (more acidic in duodenum –> ulceration) - Can see them with alcian blue toll yellow stain
- Blue little thin tic tacs in yellow stomach
antibiotics + PPI
long term response to helicobacter infection
Long term response : mucosa changes into intestinal epithelium = intestinal metaplasia
- More resistant to acid and bugs
- Increased risk of gastric cancer (slight) . By chronic inflammation and becoming meta/dysplasia
risk factors for GORD
- Obesity and overeating – increased intraabdominal pressure!
- Hiatus hernia - stomach bulges through diaphragm hiatus
- –Rolling (paraesophageal) - 20% – Fundus of stomach prolapses through but gastroesophageal junction remains intact. Reflux less common
- – Sliding - 80% – Both gastro-oesophageal junction and part of stomach slide up into chest through the hiatus. Reflux more common as the sphincter is less competent
- Smoking
- Alcohol
- Pregnancy
- Systemic sclerosis
pathophysiology of GORD
inc normal and resulting histology
Should be a clear junction between oesophagus and stomach
- Oesophagus = squamous epithelium (for abrasion eg crisps)
- Stomach = glandular epithelium (acid secretion + mucin layer)
- Lower oesophageal sphincter relaxes more transiently and frequently, not only following swallowing to allow bolus entry into the stomach
- Lower oesophageal sphincter may have less tone
- Acid reflux through the lower oesophageal sphincter causes the oesophageal cells to die quickly because the squamous cells have no mucin barrier
- Ulceration
- Pain
- Continued acid reflux means that this squamous epithelium cannot regrow
- Instead: metaplasia
- This is a stem cell change rather than the individual squamous cells themselves
- Now there is glandular epithelium in the oesophagus and it is covered with the associated secreted mucin layer
- This protects it from acid reflux
presentation GORD
- Weight loss maybe
- Haematemesis = vomiting blood
- Anaemia from iron deficiency
- Pain
- Heartburn = middle of chest
- Burping
- Painful swallowing = odynophagia
- Cough , hoarse voice
- Bad breath, unpleasant taste in mouth
- Feel sick
- May be triggered by particular foods
GORD histological change
oesophagus : squamous epithelium to glandular epithelium covered with associated mucin layer (like in stomach)
GORD investigations
Endoscopy
- If palpable mass, vomitting, GI bleed, dysphagia, weight loss, haematemesis, persistant symptoms (4w), old (55)
- Normal oesophagus (squamous over oesophageal mucus gland) reflects light - white/pale pink
- Barrett’s oesophagus = columnar lined lower oesophagus (CELLO) = redder, less reflective. This is glandular mucosa overlying oesophagus mucus gland
- Biopsy this
Barium swallow
- May show hiatus hernia
GORD management non iatric / advice
- Encourage weight loss
- Smoking cessation
- Small, regular meals
- Avoid: hot drinks, alcohol, citrus fruits, spicy foods, eating 3h before bed
- Raise bed head
GORD management surgical
Nissen fundoplication = increases the resting lower oesophageal sphincter pressure
- If not responding to therapy
- May cause bloating and dysphagia
GORD management pharmacological
drugs
and which to avoid
Antacids
- Eg magnesium/aliginate containing
- Reduce reflux with ‘foam raft’
PPI
- Eg lansoprazole
- Reduces gastric acid production
Avoid drugs that lower oesophageal motility
- Nitrates
- Anticholinergics
- CCB
H2 antagonist
- ranitidine
- not 1st line
AVOID drugs that damage the mucosa
- NSAIDs
- Potassium salts
- Bisphosphonates
GORD complications
Barrett’s oesophagus
- Hiatus hernia always present
- Oesophageal cancer. The dysplastic epithelium can become neoplastic epithelium == adeniocarcinoma
Peptic stricture
- Inflammation of oesophagus (oesophagitis) resulting from gastic (peptic) acid
- Gradually worsening intermittent dysphagia
Iron deficiency
Ulcers
Mallory weiss tear (in mucosa at eosophagogastric junction)
cancer of upper/ lower GI
which cancer is v rare
upper - oesophageal , stomach
(Small bowel rare)
lower - colorectal
oesophageal cancer
- commonness
- age
- gender
- Increasing frequency
- — Obesity increasing
- — reclassification from upper gastric → oesophageal cancers
- Not as common as colon cancer
- M >f
- Peaks in 60s/70s
gastric cancer
- commonness
- age
- gender
- where in world
- Incidence decreasing
- — May be due to reclassification from upper gastric → oesophageal cancers
- M >f
- E europe
- E asia
- Peaks in 70s
large bowel cancer
- gender
- age
- where in world
- commonness
- M > f
- Old age- 60/70. Rare under 30
- HICs eg N europe , rather than asia/africa
- Incidence rising with time
- Colorectal is v common
risk factors for oesophageal cancer
= risk factors for reflux/ GORD :
- Obesity – Increased intraabdominal pressure!!
- Hiatus hernia - stomach bulges through diaphragm hiatus
- – Rolling (paraesophageal) - 20%. Fundus of stomach prolapses through but gastroesophageal junction remains intact. Reflux less common
- – Sliding - 80%. Both gastro-oesophageal junction and part of stomach slide up into chest through the hiatus. Reflux more common as the sphincter is less competent
- Smoking
- Alcohol
- Pregnancy
- Systemic sclerosis
types of hiatus hernia
Hiatus hernia - stomach bulges through diaphragm hiatus
Rolling (paraesophageal) - 20%
- Fundus of stomach prolapses through but gastroesophageal junction remains intact
- Reflux less common
Sliding - 80%
- Both gastro-oesophageal junction and part of stomach slide up into chest through the hiatus
- Reflux more common as the sphincter is less competent
gastric cancer risk factors
- Smoking
- Smoked food
- Pickled food
- High salt/nitrates in diet
- Genetic, family history
- Helicopacter pylori
- – Causes chronic gastritis
- – Can lead to atrophic gastritis → metaplasia → dysplasia → cancer
- Pernicious anaemia
decreased risk: Low salt Non-starchy veg Fruit Garlic
small bowel cancer
- commonness
- risk factors
- types
- symptoms
- investigations
- treatment
rare
coeliac
crohns
(not UC- doesnt pass caeco-ileal valve)
adenocarcinoma
non-hodgkins lymphoma
anaemia, weight loss, diarrhea, pain, mass, anorexia
endoscopy and biopsy, CT/US
radiotherapy
resection
colorectal cancer genetic risk factors
Genetic predisposition:
- Familial adenomatous polyposis (FAP) = born with lots of polyps (100s-1000s)
- – Apc gene keeps beta catenin levels low
- – Apc mutation→ (misfolding)→ beta catenin levels rise → epithelial proliferation → adenoma
- – Dominant inheritance
- – May be given a prophylactic colectomy and ileorectal anstamosis
- Lynch syndrome : Hereditary nonpolyposis colorectal cancer (HNPCC)
- – No DNA repair protein produced (hMSH2/hMSH1)
- – Increased risk of damage so increased risk of cancer development - DNA damage accumulates
- – Identifying this is important: relatives’ cancer, and doesn’t respond well to chemo - so saves patients the side effects for little gain
- – Polyps develop into cancer more rapidly (normally 10y)
colorectal cancer non genetic risk factors
- adenomas
- Low fibre diet
- – Better = veg, milk, garlic, - exercise
- Sugar
- Alcohol
- Smoking
- Obesity
- Age
- Conditions
- – UC
- – Primary sclerosing cholangitis (PSC)
two types of oesophageal cancer
Adenocarcinoma : Continued acid reflux
- Affects lower ⅓ of oesophagus!!
- This causes change in epithelium → meta → hyper plasia meaning there is glandular epithelium in the oesophagus (stem cell change)
- This can develop to NEOPLASTIC glandular epithelium
Tumour can
- Protrude into lumen of oesophagus – Dysphagia
- If goes along oesophagus wall – Difficult to resect
- If goes outward into surrounding structures – may compress/ enter lymph/ vascular channels / trachea/bronchi (Small vessels quite near and vena cava/ aorta further but not miles off)
squamous cell carcinoma - v common in china, SE asia, ethiopia risk factors - Smoking - Drinking - Obesity - Low fruit/veg low prognosis Upper ⅔ of oesophagus
gastric cancer
- type of cancer
- types, and their features
- Adenocarcinoma as well (As oesophageal)
- Stomach changes to intestinal metaplasia, then dysplasia
- Then intramucosal carcinoma and then invasive carcinoma
Intestinal
- well formed, well differentiated heaped up, ulcerated lesions
- Distal stomach
- Environmental association
Diffuse
- Poorly cohesive undifferentiated cells
- Infiltrate gastric wall
- Any part of stomach, esp cardia
- Worse prognosis
gastric cancer staging
In situ = only in mucosa
Early gastric cancer = into submucosa only
- May or may not have spread to lymph nodes
- This is good prognosis, but is rare as often caught having spread further
- This is invasive. As soon as it leaves the mucosa, it is invasive
- May appear as a shallow ulcer
Late gastric cancer = into muscular wall
- +/- lymph nodes
- Linitus plastica = “leather bottle stomach” = Rigid , doesn’t move, Thickened wall, Cancer all the way through
colon cancer
- where
- how does where affect prognosis
- type of cancer
- Anywhere in colon - most in distal end !
- The proximal ones have a worse prognosis !
- Adenocarcinoma (glandular)
colon cancer staging
- dukes
- tnm
Do in lab (histopathology) at margins
Dukes A - mucosa/submucosa B - bowel wall (muscular) C - lymph nodes --- High tide lymph node = lymph node on the mesentery that is furthest from the colon D - metastases
pT pN // TNM system
Pt1- no deeper than submucosa (stage 1)
Pt2 - in muscularis propria but no further (stage 1)
Pt3 - has exitted muscularis ( to serosa/fat/lymph nodules) (stage 2)
Pn1 - 1-3 lymph node metastases(stage 3)
Pn2 - 4+ lymph node metastases (stage 4)
M - distant metastases ( stage 4)
colorectal cancer presentation
classic cancer signs
blood/mucus in poo (the nearer the cancer to the anus, the more visible these will be)
bowel habit change - diarrhea
abdom pain
gastric cancer presentation
classic cancer signs
vom/ naus/ anorexia
dysphagia if tumour in fundus
oesophageal cancer presentation
classic cancer signs
progressive!! dysphasia – solids first, then liquids (if sudden liquids and solids difficulty from beginning- indicates benign disease eg leiomyomas. these are slow growing, narrowing the lumen)
GI cancer investigations
Endoscopy + Biopsy
- Rule out pathogens
Barium meals (uses contrast) - To see strictures
CT/MRI/PET
- May show bowel wall thickening
- May show lymph node involvement (lymphoma)
- For tumour staging
- PET esp for metastases
Colorectal - Faecal occult blood (FOB) - screening - Fbc - microcytic anaemia - Colonoscopy is best Biopsy , polyps removal - Barium enema - contrast CT - better for the elderly
GI cancer management
All
- Palliative care
- Pain relief
- Chemotherapy /radiotherapy if is spread
- Surgical resection (endoscopic/surgical)
Then look in the lab at resection margins – is all cut out? RO= completely resected locally, R1 = microscopic involvement of margin by tumour R2 =macroscopic involvement of margin by tumour
- Monitor to see if any development
- oesophagus stenting allows swallowing
- radiotherapy good for small bowel
- rectal cancer hard to remove (chemo/surgery)
coeliac first line investigation
IgA TTG
small bowel histology also NEEDED for diagnosis, but isnt first line
