GI, pancreas, liver etc Flashcards
what types of cell make up the lining of the oesophagus?
squamous epithelial
non-keratinised
what are the sphincters at either end of the oesophagus called?
upper end = cricopharyngeal
lower end = gastro-oesophageal
how long is the oesophagus?
how much of the distal oesophagus is lined by glandular (columnar) mucosa? (ie distal to squamo-columnar junction)
what is the normal distance from the incisors to the squamo-columnar junction?
25 cm long
distal 1.5-2cm
40cm
what are the three main layers of the lining of the oesophagus?
what are the three sub-layers within the most superficial layer?
mucosa:
- epithelium (stratified squamous) - basal cell layer at bottom!
- lamina propria
- muscularis mucosae
submucosa
muscularis propria
oesophagitis:
- main infectious causes? 3 (with examples)
- main chemical causes? 2
infectious:
- viral (HSV1, CMV)
- fungal (candida)
- bacterial
chemical:
- reflux of gastric contents (most common!)
- ingestion of corrosive substances (mainly kids or self-harming adults)
on endoscope examination, what do these oesophageal infections look like:
- candida?
- herpes simplex?
candida = white plaques
herpes simplex = well-defined ulcers
what are the risk factors for reflux oesophagitis? 6
what is the commonest presenting symptom?
- obesity
- male
- defective lower oesophageal sphincter
- hiatus hernia
- increased intra-abdominal pressure
- increased gastric fluid volume (due to gastric outflow stenosis)
‘heart burn’
what is a hiatus hernia
what are the two different types of hiatus hernia?
what do they each tend to present with?
abnormal bulging of a portion of the stomach through the diaphragm
sliding hiatus hernia
- cardia bulges up
- reflux symptoms
paraoesophageal hiatus hernia
- fundus bulges up
- strangulation (can lead to necrosis + perforation)
what do the cells in reflux oesophagitis tend to look like (compared to normal)?
- basal cell hyperplasia
- increased inflammatory cells
basically more purple nuclei and less squamous cells
what are the potential complications of reflux oesophagitis? 5
- ulceration
- haemorrhage (at base of ulcers)
- perforation (if ulcer penetrates through wall)
- benign stricture
- BARRETT’S OESOPHAGUS
barrett’s oesophagus:
- cause?
- risk factors?
- macroscopy?
- histology?
cause:
- longstanding gastro-oesophageal reflux
risk factors:
- same as for reflux
macroscopy:
- proximal extension of squamo-columnar junction
histology:
- squamous mucosa replaced by columnar mucosa (called: glandular metaplasia)
what are the two types of barrett’s oesophagus? how do they differ?
normal barrett’s oesophagus
- no goblet cells
specialised barrett’s opoesophagus
- presence of goblet cell (norm found in small bowel)
what type of cancer can patient’s with barrett’s oesophagus develop?
- describe the 4 stages of this progression
how is this prevented?
adenocarcinoma of oesophagus
- barrett’s
- > low-grade dysplasia
- > high-grade dysplasia
- > adenocarcinoma
regular endoscopies
- freq determined by height of barrett’s + level of dysplasia
nb vast majority of people with barrett’s won’t get cancer!
what are the 2 main types of oesophageal cancer?
what are the:
- risk factors?
- geographical distribution?
- distribution in oesophagus?
adenocarcinoma
- risk factors: barrett’s, men, (maybe smoking, obesity)
- mainly caucasians
- mainly lower oesophagus
squamous carcinoma
- risk factors:
- –tobacco (main one)
- –alcohol
- –diet
- –thermal injury (very hot drinks)
- –human papilloma virus
- –male
- –black ethnicity
- mainly developing world
- middle + lower third (occasionally upper third)
what are the three different types of macroscopic appearance of oesophageal cancers?
- polypoidal (ie a lump)
- stricturing
- ulcerated
what staging system is used for oesophageal cancer?
TNM
(tumour, nodes, metastases)
nb in oesophageal cancer, ‘T’ focuses on depth of invasion through oesophageal wall
4 anatomic regions of stomach?
3 histological regions of stomach?
anatomic:
- cardia
- fundus
- body
- antrum
histological:
- cardia
- body
- antrum
nb body and fundus are histologically the same
what are the causes of gastritis due to:
- ‘increased aggression’? 7
- ‘impaired defenses’? 5
‘increased aggression’:
- excessive alcohol
- drugs (esp NSAIDs)
- heavy smoking
- corrosive
- radiation
- chemotherapy
- infection
‘impaired defenses’
- ischaemia (poor blood supply to stomach)
- shock (poor blood supply to stomach)
- delayed emptying (due to mass or stricture)
- duodenal reflux
- impaired regulation of pepsin secretion
what are the three most common causes of acute gastritis?
what are the possible complications? 2
- drugs (eg NSAIDs)
- alcohol
- initial response to helicobacter pylori infection
- erosion
- haemorrhage
nb generally heal quickly (if cause is removed)
what are three main causes of CHRONIC gastritis?
autoimmune
- anti-parietal + anti-intrinsic factor antibodies
- -> atrophy in gastric mucosa
bacterial infection (helicobacter pylori)
- majority get no disease
- 2-5% get gastric ulcers
- 10-15% get duodenal ulcers
chemical injury (NSAIDs, bile reflux, alcohol)
“ABC = causes of chronic gastritis”
what is MALT?
mucosa-associated lymphoid tissue
helicobacter pylori:
- type + shape of bacterium?
- where found in stomach?
- what does it result in, in stomach? 3
- gram negative
- spirillus
more common in antrum than body
- antrum is less acidic
- glandular atrophy
- replacement fibrosis
- intestinal metaplasia
what is the definition of a peptic ulcer?
at which 3 sites are they most common?
localised defect extending, at least, into SUBMUCOSA
- distal oesophagus (DOJ)
- junction of antral + body mucosa
- first part of duodenum
basically anywhere on the junction between different cell types
what are the main 5 causes of peptic ulcer disease?
- H.pylori infection
- duodeno-gastric reflux
- hyperacidity
- drugs (NSAIDs)
- smoking
ACUTE gastric ulcers:
- what 3 things make up ulcer slough? (which ulcers are covered in)
- what is found at the floor of the ulcer?
ulcer slough
- necrotic debris
- fibrin
- neutrophils
- granulation tissue
what is the histology of a CHRONIC gastric ulcer?
- clear-cut edges overhanging the base
- extensive granulation + scar tissue at ulcer floor
- scarring often throughout the entire gastric wall (with breaching of the muscularis propria)
- bleeding
what are the 4 major complications of peptic ulcers?
- haemorrhage (acute and/or chronic -> anaemia)
- perforation -> peritonitis
- penetration into an adjacent organ (ie fistula) - liver, pancreas
- stricturing (due to fibrosis) -> hour-glass deformity
gastric vs duodenal ulcers:
- relative incidence?
- acid levels?
- % caused by h. pylori?
duodenal 3 times more common
gastric: normal or low acid levels
duodenal: high or normal acid levels
gastric: 70%
duodenal 95-100%
what is the most common type of gastric cancer?
what are the 3 less common types?
adenocarcinoma
- endocrine tumours
- MALT lymphomas
- stromal tumours (GIST)
what is stroma?
Stroma is the part of a tissue or organ that has a connective and structural role. It consists of all the parts which do not conduct the specific functions of the organ, for example, connective tissue, blood vessels, nerves, ducts, etc. The other part is the parenchyma, which is the cells that perform the function of the tissue or organ
what are the 5 major causes of gastric adenocarcinoma?
- helicobacter pylori infection (most common)
- diet (smoked/cured meat or fish, pickled veg)
- bile reflux
- hypochlorhydria (ie low gastric acid, allows bacterial growth)
- hereditary (about 1%)
what are the differing aetiologies of gastric adenocarcinoma of the:
- Gastro-oesophageal junction (GOJ)?
- Gastric body/antrum?
GOJ: - white males - association with GO reflux - increasing incidence (due to obesity) (- no association with H. pylori/diet) - basically same risk factors as barrett's!
body/antrum: - association with H. pylori - association with diet (salt, low fruit + veg) - decreasing incidence (- no association with reflux)
what is linitis plastica?
what cause of gastric cancer is this associated with?
Diffuse type carcinoma – no distinct mass as cancer spread throughout, entire stomach wall is thickened
hereditary diffuse type gastric cancer (HDGC)
- tend to get gastric cancer in young adults + middle age
coeliac disease:
- what molecule is this a reaction to?
- what is the pathophysiology?
gliadin (component of gluten)
gliadin induces epithelial cells to express IL-15 (interleukin-15)
-> IL-15 produced by epithelium -> activation/proliferation of CD8+ intraepithelial lymphocytes (IELs)
IELs are cytotoxic + kill enterocytes
define the findings/symptoms in these different types of coeliac patient’s:
- silent disease?
- latent disease?
- symptomatic? 4
silent disease:
- positive serology
- villous atrophy
- no symptoms
latent disease:
- positive serology
- no villous atrophy
- no symptoms
symtpomatic disease:
- anaemia
- chronic diarrhoea
- bloating
- chronic fatigue
coeliac disease:
- associated extra-GI conditions? 2
- types of cancer possibly caused by coeliac? 2
- warning sign (red flag) of cancer?
dermatitis herpetiformis (10% of patients) - nasty itchy rash
lymphocytic gastritis +/or colitis (less common)
- like coeliac but in stomach/large bowel
- enteropathy-associated T-cell lymphoma
- small intestine adenocarcinoma
if symptoms persist DESPITE a gluten-free diet
coeliac disease:
- possible complications? 4
- diagnostic tests? 2
- treatment?
- histological findings? 4
- anaemia
- female infertility
- osteoporosis
- cancer
- serology
- endoscopy w biopsy (before + after GFD is gold standard))
gluten-free diet (GFD)
- villous atrophy
- crypt elongation
- increased intra-epithelial lymphocytes (IELs)
- increased lamina propria inflammation
what are the 2 different types of diverticulosis?
what’s the difference between them?
which is more common?
congenital (eg merkel’s diverticulum)
- all levels of the bowel wall
acquired (‘pseudo’)
- ONLY mucosa + submucosa
- more common
what are taenia coli?
longitudinal thickenings of muscularis propria
where are acquired diverticulum most commonly found
sigmoid colon
- between mesenteric + anti-mesenteric taenia coli
nb this is most common findings but can be found elsewhere
what are the 2 main risk factors for diverticular disease?
- low fibre diet
- increased age
why do diverticular pouches develop?
increased intra-luminal pressure
points of relative weakness in the bowel wall
nb connective tissue weakens as you age
what are the clinical features of diverticular disease?
what % develop acute and chronic complications?
- asymptomatic (90-99%)
- cramping abdominal pain
- alternating constipation + diarrhoea
10-30% develop complications
name 3 acute complications of diverticular disease
diverticulitis (20-25%)
- due to bacterial overgrowth
- can develop peridiverticular abscess, causing pyrexia etc - more serious
perforation, can -> peritonitis)
haemorrhage (causes rectal bleeding)
name 4 chronic complications of diverticular disease
intestinal obstruction
- due to stricturing (due to repeated infection/inflammation)
fistula
- bladder/vagina/small bowel
diverticular colitis
- infection in lumen around diverticular pouches
polypoid prolapsing mucosal folds
- can cause a bit of bleeding + diarrhoea
what are 4 common causes of acute colitis?
infective
- eg campylobacter, shigella, salmonella, CMV
antibiotic
- incl C. diff
drug-induced
acute ischaemic colitis
- transient or gangrenous
what are the 2 most common types of chronic colitis?
what are 6 rarer types?
- chronic idiopathic inflammatory bowel disease
- ischaemic colitis
less common:
- diverticular colitis
- microscopic colitis
- chronic infective colitis (eg TB)
- diversion colitis
- eosinophilic colitis
- chronic radiation colitis
what are the three different types of chronic idiopathic inflammatory bowel disease?
ulcerative colitis
crohn’s disease
unclassified + indeterminate colitis (10-15%)
- half way between UC + crohn’s
does smoking increase or decrease risk of:
- crohns?
- UC?
which one does appendectomy protect against?
name two other risk factors for both
smoking:
- crohn’s = bad
- UC = good
appendectomy protects against UC
- oral contraceptive
- FH (of either)
symptoms of UC? 7
- rectal bleeding (>90%)
- diarrhoea (66%)
- abdominal pain (30-60%)
- weight loss (15-40%)
- anorexia
- anaemia
- constipation (2%)
what are the complications of UC? 5
toxic megacolon + perforation
haemorrhage
carcinoma
primary sclerosing cholangitis (PSC) aka primary billiary cholangitis (PBC)
- inflammation + fibrosis of bile ducts -> obstructive liver problems (can lead to liver cancer)
strictures (rare, if seen rarely benign)
symptoms of crohns? 9
- diarrhoea (may be bloody)
- peri-anal disease
- colicky abdominal pain
- palpable abdominal mass (thickened bowel due to depper infiltration) - sometimes
- weight loss (failure to thrive in children) - often
- anorexia
- fever
- anaemia (often)
- oral ulcers
what are the three commonest areas of the GI tract to be affects by crohns?
- ileocolic (junction of terminal illeum + caecum)
- small bowel
- colon (hard to distinguish from UC)
what are the complications of crohns? 7
- toxic megacolon
- perforation
- fistula
- stricture (common)
- haemorrhage
- carcinoma
- short bowel syndrome
what is short bowel syndrome?
malabsorption disorder caused by a lack of functional small intestine
caused by repeated surgical resections of small bowel
primary symptom is diarrhea, which can result in:
- dehydration
- malnutrition
- weight loss
what are the 3 major and 4 minor risk factors for UC developing into colorectal cancer?
major:
- early age of onset
- duration of disease >8-10 years
- total/extensive colitis (ie beyond splenic flexure)
minor:
- presence of PSC (primary sclerosing colangitis) aka PBC
- FH of colorectal cancer
- severity of inflammation
- presence of dysplasia
name difference between UC and crohn’s.
- spread in GI tract?
- effect of smoking?
- likelihood of rectal bleeding?
- likelihood of strictures?
- layers of bowel wall affected?
- presence of granulomas?
- peri-anal disease?
spread:
- UC: continuous from rectum up
- crohn’s: patchy, anywhere in GI tract (‘skipped lesions’)
smoking:
- UC: makes better
- crohn’s: makes worse
rectal bleeding:
- UC: highly likely
- crohn’s: less likely
strictures:
- UC: rare
- crohn’s: common
layers affected:
- UC: just mucosa
- crohn’s: deeper infiltration
granulomas:
- UC: absent
- crohns: present in 50%
peri-anal disease:
- UC: don’t get
- crohn’s: more likely
nb both UC + crohn’s are relapsing/remitting conditions!!
what is offered to reduce risk of cancer developing?
regular colonoscopies
(after having had disease for more than 10 years)
frequency dependent on other risk factors
what is ischaemic colitis?
what are the 2 subtypes?
what conditions is it associated with?
colonic injury secondary to an acute, intermittent of chronic reduction in blood flow
- occlusive (blood flow blocked completely)
- non-occlusive (blood flow reduced)
nb varies from mild (80%) to severe (15%)!!
other vascular diseases, eg:
- hypertension
- peripheral vascular disease
- coronary artery disease
- diabetes mellitus
- chronic renal failure
- COPD
what are the symptoms of ischaemic colitis? 3
- acute onset cramping abdominal pains
- urge to defecate
- bloody diarrhoea/ rectal bleeding
nb in majority (mild) symptoms improve within 48hours (completel recovery within a fortnight)
nb 20% require surgery for colonic infarction
where in the large bowel are you most likely to get ischaemic colitis? why?
just distal/proximal to the splenic flexure
as this is a watershed between the superior mesenteric artery (SMA) and the inferior mesenteric artery (IMA)
when do haemorrhagic infarctions occur?
when there’s a blockage in a large vein so blood backs up, pressure builds -> haemorrhage
what is a colorectal polyp?
what is it called when there are multiple?
what are the 3 morphological types?
a mucosal protrusion
polyposis
- pedunculated (have a stalk, bit like mushroom)
- sessile (no stalk)
- ‘flat’
what are 6 types of non-neoplastic polyps?
- hyperplastic polyps (most common)
- hamartomatous polyps
- polyps related tomucosal prolapse
- post-inflammatory polyps (see in IBD after inflammation)
- inflammatory fibroid polyp
- benign lymphoid polyp
hyperplastic polyps:
- where common in GI tract?
- what subtype may give rise to cancer?
rectum + sigmoid colon
- 1-5mm in size
- often multiple
sessile serrated lesions
- large
- found on RIGHT colon
- can give rise to microsatellite unstable carcinoma
juvenile polyps:
- type of polyp?
- morphology of polyp?
- where occur in GI tract?
- cancer risk?
- presentation?
hamartomatous
pedunculated (+ spherical head)
rectum + distal colon
sporadic: no malignant potential
genetic: increased risk of cancer (=juvenile polyposis)
- diarrhoea + rectal bleeding
nb commonest type of polyp in children
peutz-jeghers syndrome:
- type of polyp?
- where occur in small bowel?
- inheritance?
- symptoms? 4
- cancer risk?
hamartomatous
predominately small bowel
autosomal dominant
- abdo pain
- GI bleeding
- anaemia
- brown freckles around lips/oral mucosa (+ fingers?)
increased likelihood of cancers of:
- pancreas
- liver
- lung
- breast
- uterus
- ovaries
- testes
- and others
nb polyps rarely develop into cancer but mutation that causes them causes cancers in other parts of body
what are the risk factors for an adenoma (a type of neoplastic polyp) progressing into adenocarcinoma? 5
- flat adenomas (as opposed to sessile or pedunculated)
- large (>10mm)
- villous or tubulo-villous (as opposed to tubulus)
- high grade dysplasia
- if patient has lynch syndrome
colorectal cancer:
- risks? 8 (excluding lynch + FAP)
- protective things? 4
risks:
- diet high in fat
- diet high in red meat
- obesity/lack of physical activity
- alcohol
- HRT + oral contraceptives
- schistomiasis
- pelvic radiation
- IBD (UC + crohns)
protective:
- high fibre diet
- high folate diet
- high calcium diet
- NSAIDs + aspirin
what is FAP?
- inheritence?
- genetic mutation?
- colonoscopy finding?
- cancer risk?
familial adenomatous polyposis
autosomal dominant
- mutation in APC tumour suppressor gene
multiple (100s/1000s) of benign adenomatous polyps in colon
100% lifetime risk of colorectal cancer (norm get in 30s/40s)
- increased risk of other cancers too
lynch syndrome:
- another name for it?
- inheritance pattern?
- genetic mutation?
- cancer risk?
HNPCC - hereditary non-polyposis colorectal cancer
autosomal dominant
- mutations in DNA mismatch repair genes
50-70% lifetime risk of colorectal cancer
increased risk of:
- endometrial
- ovarian
- gastric
- small bowel
- urinary tract
- billary tract
what type of cancers are the vast majority of colorectal cancers?
adenocarcinomas (>95%)
what are the 5 ways in which colorectal cancers spread?
- direct invasion of adjacent tissue
- lymphatic metastasis
- haematogenous metastasis (norm to liver + lung)
- transcoelimic (peritoneal) metastasis
- iatrogenic spread (ie during biopsies etc)
what two staging systems are used for staging colorectal cancer?
TNM
dukes
angular chelitis:
- what is it?
- cause?
- most common in?
acute or chronic inflammation of the skin + next door mucosa at the corners of the mouth
- normally bilateral lesions, may be painful
excessive moisture from saliva -> maceration (breakdown of tissue from too much liquid) + secondary infection with Candida albicans (less commonly staph aureus)
- older people with dentures
- young children
dental infections
- what are caries?
- what is pulpitis?
- cause? (incl 2 organisms)
- diagnosis?
- management?
caries = tooth decay pulpitis = infection/inflammation of pulp of the tooth (where blood + nerves are) secondary to decay
acid produced by bacteria
- streptococcus mutans - “MUTAte your teeth!”
- lactobacillus spp
- examination
- dental x-rays
caries = fillings pulpitis = root canal procedure
oral hairy leucoplakia
- signs/symptoms?
- cause?
white plaques on tongue
epstein barr virus (norm give glandular fever)
- only really seen in HIV patients
