Gastroenterology Flashcards
where oesophageal star and end
C5
T10
stages of swallowing
4 (0-3)
oral
pharyngeal
upper oesophageal
lower oesophageal
sequence of stages of swallowing of the 2 shincter
CC
OO
CO
how to determine motility of oesophagus
manometery
what is LOS resting pressure / relaxation mediated by
inhibitory noncholinergic nonadrenergic neurons of myenteric plexus (NCNA)
causes of functional disorders of the oesophagus
Abnormal contractions: (Hypermobility
Hypomobility
Disordered coordination)
Failure of protective mechanisms: GORD
achalasia causes
Loss of ganglion cells in aurebach’s myenteric plexus in LOS wall
decreased inhibitory neuron activity
cannot relax properly
secondary achalasia causes
chagus disease (parasite)
protozoa infection
amyloid
What diseases is hypermotility of oesophagus seen in
Chagas disease
Protozoa
Amyloid
Sarcoma
Eosinophilic oesophagitis
what is achalsia
increased resting pressure of LOS
relaxation too late or weak
swallowed food collects in oesophagus cause increased pressure throughout with dilation of oesophagus
achalasia treatment
pneumatic dilation (PD)
to weaken LOS by circumferential stretching to stretch muscles of LOS
what is heller’s myotomy
A continuous myotomy performed for 6cm on the oesophagus and 3 cm onto the stomach
split the muscle
treatment of achalasia
What is dor fundoplication
partial wrapping of the stomach around the esophagus to make a low-pressure valve) performed to prevent reflux from the stomach into the esophagus following the myotomy.
risks of heller’s myotomy and dor fundoplication
oesophageal and gastric perforation
vagus nerve division
splenic injury
what is scleroderma
autoimmune
hypomotility in early stages
atrophy of smooth muscles of oesophagus
reduced resting pressure of LOS
CREST syndrome
what is CREST syndrome
calcinosis,
Raynaud’s
esophageal dysmotility, sclerodactyly,
telangiectasia
what is corkscrew oesophagus
diffuse oesophageal spasm
incoordinate contractions
dysphagia and chest pain
treatment for corkscrew oesophagus
forceful PD of cardia
how to find iatrogenic oesophageal perforation
oesophagogastroduodenoscopy (OGD)
what is Boerhaave;s oesophageal perforation
sudden increase in intra-oesophageal pressure with negatvie intro thoracic pressure
what is foriegn body oesophageal perforation
disk batteries (cause electric burn if in mucosa)
magnets
sharp objects
dishwasher tablet
acid/alkali
what is trauma type oesphageal perforation
neck = penetrating
thorax = blunt force
clinical features of trauma type oesopheal perforation
dysphagia
blood in saliva
haematemesis
surgical empysema
types of oesphageal perforation (4)
iatrogenic
trauma
foreign body
Boerhaave’s
where are the areas of oesophagus prone to perforation
cricopharyngeal constriction
aortic and bronchial constriction
diaphragmatic and sphincter constriction
management for oesophageal perforation
IV fluids
borad spectrum AB
bloods (G&S)
definitive management for oesophaeal perforation (2)
conservative management with covered metal stent
operative management (primary repair is optimal, oesophagectomy is definitive)
why LOS usually close
act as barrier to against reflux of harmful gastric juice (pepsin and HCl)
what are the mechanisms of protection after reflux (3)
volume clearance (oesophageal peristalsis reflux)
pH clearnace
epithelium (barrier properties)
mechanism of inhibiting reflux
Ach, alpha adrenergic agonists cause increased pressure in oesophageal sphincter
cause inhibition of reflux
mechanism of promoting reflux
Beta adrenergic agonists, dopamine NO, gastric juice, fat cause decreased pressure in oesophageal sphincter
promote reflux
what happens if fail to protect oesophageal
GORD
stOmach acid leaks up into oesophagus
causes of GORD
reduced sphincter pressure
reduced saliva production cause pH clearance
abnormal peristalsis cause volume clearance
What increases LOS pressure
Acetylcholine
Alpha-adrenergic agonists
Hormones
Protein-rich food
Histamine
High intra-abdominal pressure
INHIBITS REFLUX
what decreases LOS pressure and promotes
acidic food
fats
NO
smoking
What are sliding hiatus hernias
involve both lower oesophagu and stomach
portion of stomach herniated
ligament holding the distal oesophagus down gives way so whole stomach slides up into chest
What is a rolling hiatus hernia
portion of stomach sticks upside
Junction is in place and the stomach herniates alongside the oesophagus
How do you investigate GORD (3)
- OGD - to exclude cancer
or confirm oesophagitis, peptic stricture and barretts - Oesophageal manometry
- 24hr oesophageal pH recording
GORD treatments
lifestyle changes
PPIs
dilation peptic stricutres
laproscopic Nissen’s fundoplication
what is erosive and haemorrhagic gastritis
acute ulcer
gastric bleeding and perforation
what is nonerosive chronic active gastritis and its treatment
helicobacter pylori (H.pylori)
PPi
Triple treatment (amoxicillin, clarithromycin, pantoprazole)
what is atrophic gastritis
fundus
autoantibodies vs part and products of parietal cells
parietal cells atrophy
reduce acid and IF secretion
neural stimulation of gastric secretion
Ach
postganglionic transmitter of vagal parasympathetic fibres
endocrine stimulation of gastric secretion
gastrin
from G cells of antrum
Paracrine stimulation of gastric secretion
Histamine (ECL cells and mast cells of gastric wall)
Endocrine inhibition of gastric secretion
secretin from S.I
paracrine inhibition of gastric secretion
somatostatin (SIH)
paracrine and autocrine inhibition of gastric secretion
PGs
TGF-alpha
adenosine
What are the different types of gastritis (4)
erosive and haemorrhagic
Nonerosive, chronic active gastritis
Atrophic (fundal gland) gastritis
Reactive gastritis
methods of mucosal protection in stomach (4)
Mucus film
HCO3- secretion
Epithelial barrier (tight junctions, strong apical membrane)
Mucosal blood perfusion (good blood supply can get rid of H+ quickly)
what is produced in the cardia and pyloric region
mucus
what is produced in the body and fundus
mucus
HCl
pepsinogen
what is produced in the antrum
gastrin
what are the mechanisms for repairing epithelial defects (epithelial repair and wound healing)
- migration
- gap closed by cell growth (stimulated by EGF, TGF-alpha, IGF-1, GRP, gastrin)
- acute wound healing (BM destroyed and attract leukocytes, macro[hages, phagocytosis of necrotic ells, angiogenesis, regenration fo ECM)
How does migration repair epithelium
Adjacent epithelial cells flatten to close gap
via sideward migration along BM
how are ulcers formed
H. Pylori
Increased gastric juice secretion
Decreased bicarbonate secretion
Decreased cell formation
Decreased blood perfusion
medical treatment for ulcer
PPI or H2 blocker
Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
clinical outcomes for H.Pylori infection
- asymptomatic or chronic gastritis
- chronic atrophic gastritis, intestinal metaplasia
- gastric or duodenal ulcer
- gastric cancer
surgical treatment for ulcer and medical follow up
Intractability after medical therapy
continuous requirement for steroid therapy / NSAIDS
complications of surgical treatment for ulcer
haemorrhage
obstruction
perforation
When would you opt for elective surgery for ulcers
Rare - most uncomplicated ulcers heal within 12 weeks
if not - change medication, observe additional 12 weeks
Check serum gastrin (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison syndrome])
OGD: biopsy all 4 quadrants of ulcer (rule out malignant ulcer) if refractory
where are osmorecceptors found in hypothalamus (2)
organum vasculosum of lamina terminalis (OVLT)
subfornical organ (SFO)
how angiotensin ll affects ADH secretion
increase
and increase thirst as well
what is ghrelin responsible for
hunger hormone
increase appetite
what is leptin for
inhibit hunger
what is appetite stimulant signal described as
orexigenic
what is appetite suppressive signal described as
anorectic
which part of hypothalamus release orexigenic signal
lateral hypothalamus (feeding centre)
which part of hypothalamus release anorectic signa;
ventromedial hypothalamus (satiety centre)
what happens to lesion in ventromedial hypothalamus (satiety centre)
obesity
what nucleus in hypothalamus release oxytocin and ADH
paraventricular nucleus
what signals does arcuate nucleus in hypothalamus contain
orexigenic and anorectic signals
how is the BBB in arcuate nucleus and why is it in this way
incomplete
to allow access to peripheral hormones
main role of arcuate nucleus in hypothalamus
regulation of food intake
what are the 2 neurone populations in arcuate nucleus
stimulatory (NPY/AGPR neurone)
inhibitory (POMC neurone)
what happens to activation of POMC neurone
inhibit food intake
which receptor is highly expressed in paraventricular nucleus
MCR receptor
how melanocortin system reduce appetite
arcuate nucleus release POMC neurone
POMC cause increase in α– Melanocyte-stimulating hormone (alpha MSH)
alpha MSH increase bind to MC4R in paraventricular nucleus to reduce food intake
how melanocortin system increase appetite
arcuate nucleus release AgRP
cause inhibition in MC4R
increase food intake
what is the mechanism in regulating food intake
fat produces circulating hormone
hypothalamus senses the concentration of hormone
then alters neuropeptides to increase/decrease food intake
where does leptin acts on
hypothalamus
role of leptin
regulate appetite (intake) and thermogenesis (expenditure)
where is leptin secreted from (2)
white adipose tissue and gastric mucosa
low level of leptin indicates what
low body fat
high level of leptin indicates what
high body fat
what is leptin resistance
leptin is present but doesn’t signal effectively
where are gut hormones that regulate appetite released
enteroendocrine cells in stomach, pancreas, small bowel
which gut hormones inhibit appetite
peptide YY (PYY)
glucagon like peptide -1 (GLP-1)
which gut hormone increase appetite
ghrelin
how does ghrelin prepare food intake in gut
increase gastric motility and acid secretion
how ghrelin modulates neurone in arcuate nucleus
stimulate NPY/ AgRP neuornes to increase appetite
inhibit POMC neurone
what is ghrelin involved in
increase appetite
regulation of rewards
taste sensation
memory
carcadian rhythm
when is PYY released
in response to feeding
where is PYY released
terminal ileum and colon
effect on PYY on arcuate nucleus
stimulate POMC
inhibit NPY
overall reduce appetite
when is GLP-1 released
response to feeding
effect of GLP-1in appetite
reduces appetite
GLP-1 effects to stomach, liver, pancreas, adipose tissue, heart, brain
stomach: decrease gastric empyting
liver: reduce glucose production
pancreas: increase insulin secretion, reduce glucagon, increase insulin biosynthesis, increase B cell proliferation and reduce apoptosis
adipose tissue: increase glucose uptake and storgae
heart: increase cardiac function and protection
brain: increase neuroprotection and reduce appetite
what organs are associated wit right hypochondriac region (2)
gallbladder
liver
what organs are associated wit left hypochondriac region
pancreas
what organs are associated wit epigastric region
stomach
duodenum
pancreas
what organs are associated wit right and left lumbar region
kidney
what organs are associated wit umbilical region
small bowel
what organs are associated wit right iliac region
appendix
caecum
what organs are associated wit left iliac region
sigmoid colon
what organs are associated wit hypogastric region
bladder
uterus
adnexae
describe the character of pain that produced by kidney stone
colicky
describe the character of pain that produced by liver
constant
describe the character of pain that produced by spleen
constant
radiation of pain that you’d expect produced by gallbladder
upper right quadrant through to back and to right
radiation of pain that you’d expect produced by pancreas head
straight to back and left
radiation of pain that you’d expect produced by pancreas tail
through to back and left
radiation of pain that you’d expect by kidney
in loin and radiates to groin
radiation of pain for small bowel
doesn’t radiate
what does tolerance mean in GIT immunology
cell absorb pathogen and form immune response through food antigens and commensal bacteria
what is dual immunological role in gut immunology
if too much activation, won’t go to tolerance phase and go to activation phase
what are the 4 main bacteria in gut
bacteroidota
firmicutes
actinobacteria
proteobacteria
what microbiota are in gut
bacteria
virus
fungi
what does symbiosis mean
living tgt
without benefit or harm each other
what are commensals
a microorganism which benefits from association but no harm to host
what are pathobionts
symbiont doesn’t normally hv inflammatory response but under some conditions has the potential to cause dysregulated inflammation and disease
what is dysbiosis
altered microbiota composition, turn healthy microbiota to inflammatory response
causes of dysbiosis
infection or inflammation
diet
xenobiotics
hygiene
geentics
examples of bacterial metabolites and toxins in dysbiosis
TMAO
4-EPS
SCFAs
bile acids
AHR ligands
what is gnotobiogy
absence of microorganisms / germ free will cause hindered development of short intestine
results in reduced peyer’s patches for immune response
what are some immunological ways after invasion to protect body from gut invasion (2)
MALT (mucosa associated lymphoid tissue)
GALT (gut associated lymphoid tissue)
what are on the gut epithelial barrier to help defence bacteria (3)
mucus layer (goblet cells)
epithelial monolayer (tight junctions)
paneth cells (small intestins)
where are paneth cells found
crypts of lieberkuhn
roles of paneth cells
secrete antimicrobial peptides (help with digestions) and lysozyme
in MALT where are HEVs (high endothelial venules) found
lymph nodes
secondary lymphoid organs
not in spleen
in MALT what are lymphoid follicles surrounded by
high endothelial venules postcapillary venules
importance of HEVs (3)
immune surveillance (identify foreign invaders and changes in body’s own cells eg neoantigens in cancer)
lymphocyte recirculation (support high levels of lymphocyte extravasation from blood)
immune response (help inititae and maintain immune response in lymph nodes)
is the oral cavity rich in immunological tissue
yes
eg pharyngeal tonsil
in GALT , what immune responses are results of generations of lymphoid cells and antibodies
both adaptive and innate immune responses
in GALT, what are the non-organised /1st line attack in immune response
intra-epithelial lymphocytes (T cells, NK cells)
lamina propria lymphocytes
in GALT, what are the organised /1st line attack in immune response
peyer’s patches (Small intestine)
caecal patches (Large intestine)
isolated lymphoid follicles
mesenteric lymph nodes
what are peyer’s patches
specialised nodules in ileum
mainly distal ileum
which has more microbiota, peyer’s patches and surface area for immunological response (small or large intestine)
small
what are peyer’s patches
immune sensors
aggregated lymphoid follicles covered with follicle associated epithelium (FAE)
what are FAE (follicle associated epithelium)
no goblet cells
no secretory cells
lack microvilli
composed of specialized Immune effector cells that cover the luminal side of the lymphoid follicles of GALT
what takes up antigen within follicle associated epithelium
M cells (microfold cells)
what does M cells express in peyer’s patches
express IgA receptors to facilitate transfer of IgA bacteria complex into peyer’s patches to activate naive T and B cells
what is antigen sampling in gut
at antigen presentation, all dendritic cells that originally hide will squeeze out via tight junctions and mucosa epithelial cells to captivate antigen and relocate to mesenteric lymph nodes
is antigen sampling dependent or independent on M cells
independent route
what do B cells express in peyer’s patches
IgM
on antigen presentation what does IgM on B cells in peyer’s patches switch to
IgA
what is the B cell adaptive response in gut
naive B cells express IgM in peyer’s patches
when antigen presented, switch to IgA
T cells and epithelial cells influence B cell mturation via cytokine production
B cells mature to become IgA to secrete plasma cells
B cells populate in lamina propria
what cells secrete IgA
gut B cells to form secretory IgA (sIgA)
what do sIgA do after secreted from gut B cells
binds to luminal antigen to prevent its adhesion and invasion
what does homing cascade do in gut
directs circulating naive t cells to peyer’s patches
mechanism of homing cascade in gut
rolling of gut hormone
MAdCAM-1 adhesion and bind to tight junctions via a4B7 integrein
cause activation at HEV
arrest
do enterocytes and goblet have short or long lifespan
short
so need rapid turnover rate
why short lifespan for enterocytes and goblet cells
remove toxic substances
replace anything died off
what are enterocytes function in first line defence
against GI pathogens and directly affected by toxic substances i diet
affect cell function, metabolic rate
any lesions are short lived
how is chorela transmitted
transmitted thru faecal-oral route
spread via contaminated water and food
which bacteria cause cholera infection
vibrio cholerae serogroups O1 and O39
what happens when cholera bacteria reaches small intestine
contact with epithelium and release cholera enterotoxin
increase cAMP activity
increase ion pumps and lose water thru GIT
diarrhoea
main symptoms of cholera infection
dehydration and watery diarrhoea
how to diagnose cholera infection
bacterial culture from stool sample on selective agar
rapid dipstick tests
treatment for cholera infection
oral-rehydration
vaccine
examples of viral infection of infectious diarrhoea gastroenteritis
rotavirus
norovirus
other causes of infectious diarrhoea in gut
protozoal parasitic
bacterial
what is rotavirus
RNA virus
where does rotavirus replicate
in enterocytes
how many types of rotavirus and which is most common
5 types A-E
type A most common
treatment for rotavirus infection
oral rehydration
vaccine (live attenuated oral vaccine against Type A)
what does rotavirus cause
infectious diarrhoea
what is norovirus
RNA virus
route of transmission of norovirus
faecal-oral transmission
outbreaks often in closed communities
symptoms of norovirus infection
vomit
acute gastroenteritis
how to diagnose norovirus
sample PCR
what is campylobacter
curved bacteria
most common species:
campylobacter jejuni, campylobacter coli
route of transmission of campylobacter
undercooked meat
untreated water
unpasteurised milk
treatment of campylobacter
not usually need
but if need take antibiotic (azithromycin, macrolide)
what is E.coli
gram negative intestinal bacteria
most harmless but hv 6 pathotypes associated with diarrhoea (diarrhoeagenic)
management of C.diff bacteria
isolate patient
stop current antibiotics
take metronidazole and vancomycin
faecal microbiota transplantation
what are the investigations for GI disorders and infection
stool sample (for C.diff toxin esp those taking antibiotics)
stool culture
AXR
CT
endoscopy
control of GI disorders
need isolate or not?
continue antibiotics?
management of fluids? nutrition and diarrhoea?
which antibiotic for C.diff patients
vancomycin/
metronidazole /
fidaxomicin
which bacteria is often associated with pseudomembranous colitis
C.difficile infection
bacterial causes of infectious diarrhoea
C.diff (clostridium difficile)
shigella
Salmonella spp
E.coli
non infectious diarrhoea causes
IBD
haemorrhoids
post infectious IBD
microscopic colitis
ischaemia colitis
coeliac disease
if colonoscopy showed left sided inflammatory changes, chronic inflammation with no granulomas what are some likely diagnosis
ulcerative colitis
adipsia meaning
lack of thirst even body low on water
3 causes of primary polydipsia
dehydration
hypothalamus injury
organic brain damage
conditions that cause secondary polydipsia
DM
Diabetes insipidus
psychogenic polydipsia
Conn’s syndrome
AVP resistance
diuretics
anti-depressant
laxatives
what is conn’s syndrome
Primary aldosteronism, also known as primary hyperaldosteronism, excess production of the hormone aldosterone from the adrenal glands, resulting in low renin levels and high blood pressure.
when high aldosterone, does it associate with hyper or hypokalaemia
hypokalaemia
what are the 3 main groups that cause malnutrition in hospital
reduced intake
malabsorption / maldigestion
altered metabolism
steps to diagnose malnutrition
screening
assessed by dietician
diagnose
who are considered malnourished and need nutrition support
BMI < 18.5
unintentional weight loss of >10% in past 3-6 months
BMI < 20 + unintentaional weight loss of >5% in past 3-6 months
who are considered at risk of malnourished and need nutrition support
eaten little or nth in >5days or likely to eat nth or eat little or nth in next 5 days
poor absorptive capacity or high nutrient losses or increased nutritional needs from causes eg catabolism
what is artificial nutrition support
provision of enteral or parenteral nutrients to treat / prevent malnutrition
what does enteral mean in artificial nutrition support
utilise GIT to provide nutrient
which is more superior, enteral or parenteral nutrtion
enteral
ultimate aim of mode of feeding
return to oral feeding as soon as clinically possible
if gastric feeding possible, which tube should we use for feeding malnutrition pt
naso-gastric tube (NGT)
if gastric feeding not possible, which tube should we use for feeding malnutrition pt
naso-duodenal tube (NDT) or naso-jejunal tube (NJT)
long term artificial nutrition support enteral example
gastrostomy/jejunostomy
what are the 3 main complications area associated with enteral feeding
mechanical
metabolic
GI
mechanical complications of enteral feeding
misplaced tube
blockage
buried bumper
metabolic complications of enteral feeding
hyperglycaemia
deranged electrolytes
GI complications of enteral feeding
patient not absorb, obstruction, vomit, diarrhea, nasopharyngealmpain, laryngeal ulceration
what is parenteral nutrition (PN)
delivery of nutrients, electrolytes, fluid directly into venous blood
when to use parenteral nutrition
inadequate or unsafe oral and / or enteral nutritional intake
non-functioning, inaccessible or perforated GIT
how to access parenteral nutrition
use central venous catheter (CVC): tip at SVC and RA where nutrients are received
what are complications associated with parenteral nutrition
metabolic
mechanical
catheter related infections
where is albumin synthesised
liver
what hypoalbuminaemia indicate
increased inflammation
poor prognosis
acute phase response leading to hypoalbuminaemia
inflammatory stimulus cause activation of monocytes¯ophages
release cytokines
cytokines act on liver to stimulate synthesis of some proteins eg CRP
downregulation production of others eg albumin
what is refeeding syndrome (RFS)
a group of biochemical shifts and clinical symptoms that occur in malnourished or starved individual on reintroduction of oral, enteral, parenteral nutrition
consequences of refeeding syndrome
arrhythmia, tachycardia, cardiac arrest, sudden death
respiratory depression
encephalpathy
coma, seizures
wernicke’s encephalopathy
what is pathogenesis of refeeding syndrome
starvation/malnutrition
glycogenesis, gluconeogenesis, protein catabolism
protein, fat, mineral etc intolerance
refeed
fluid, salt, nutritents
insulin secretion
increase protein and glycogen synthesis
increase glucose uptake, utilisation of thiamine, uptake of K+, Mg2+, PO4 3-
hypokalaemia hypomagnesaemia, thiamine deficiency
what criteria are at risk of refeeding syndrome
very little or no food intake for >5days
what criteria are at high risk of refeeding syndrome
> /= 1 of the following:
- BMI < 16 kg/m2
- Unintentional weight loss > 15 % 3 – 6 months
- Very little / no nutrition > 10 days
- Low K+, Mg2+, PO4 prior to feeding
OR
/= 2 of the following:
- BMI < 18.5 kg/m2
- Unintentional weight loss > 10 % 3 – 6 months
- Very little / no nutrition > 5 days
- PMHx alcohol abuse or drugs (insulin, chemotherapy, antacids, diuretics)
what criteria are at extremely high risk of refeeding syndrome
BMI < 14 kg/m2
Negligible intake > 15 days
management of refeeding syndrome
- Administer thiamine 30 minutes before and for the first ten days of feeding following Trust policy
- Correct and monitor electrolytes daily following Trust policy
- micronutrients from onset of feeding (start 10-20cal/kg) CHO 40-50% energy
- Monitor fluid shifts and minimise risk of fluid and Na+ overload
what are the different types of cancer of GIT (6)
- squamous cell carcinoma (SCC)
- adenocarcinoma
- Neuroendocrine tumors (NET)
- Gastrointestinal Stromal Tumors (GISTs)
- leiomyoma/leiomyosarcomas
- Liposarcomas
different forms of colorectal cancer (3)
sporadic
familial
hereditary syndrome
what causes normal epithelium transform to hyperproliferative epithelium in colorectal cancer (4) + what mutation
aspirin and NSAIDS
folate
calcium
APC mutation
COX-2 overexpression cause aberrant cryptic foci
what causes hyperproliferative epithelium transform to small adenoma in colorectal cancer (2)
aspirin
NSAIDS
what causes small adenoma transform to large adenoma in colorectal cancer (3)+ what mutation
oestrogen
aspirin
NSAIDS
K-ras mutation
what mutation and loss of what cause large adenoma change to colon carcinoma
p53 mutation
loss of 18q
clinical presentations in caecal and right sided cancer
iron deficiency anaemia
change in bowel habit (diarrhoea)
distal ileum obstruction (late)
palpable mass (late)
clinical presentations in left sided and sigmoid carcinoma
rectal bleeding
mucus
thin stool (late)
clinical presentations in rectal carcinoma
rectal bleeding
mucus
tenesmus
anal, perineal, sacral pain(late)
bowel obstruction (late)
metastasis of colorectal cancer clinical presentation (4 areas)
liver (hepatic pain, jaundice)
lung (cough)
regional lymph nodes
peritoneum (sister marie joseph nodule)
signs of primary colorectal cancer in examination
abdominal tenderness and distension (large bowel obstruction)
rigid sigmoidoscopy
abdominal mass
digital rectal exam (<12cm dentate and reached by examining finger)
sings of metastasis and complications of colorectal caner
hepatomegaly
monophonic wheeze
bone pain
colorectal cancer investigation for faecal occult blood
FIT (faecal immunochemical test)
guaiac test (based on pseudoperaoxidase activity of haematin)
blood tests for colorectal cancer
FBC
tumor markers
investigations for colorectal cancer (imaging)
CT colonoscopy
colonography
investigations for rectal cancer (imaging)
MRI pelvis
what are CT Chest/ abdo/ pelvis scans for in colorectal cancer
staging prior treatment
main management of colon cancer
stent
radiotherapy
chemo
2 main types of obstructive colon carcinoma
right and transverse colon
left sided obstruction
which artery supply all small bowel
SMA
what’s the name of the procedure to remove one side of the colon
hemicolectomy
aetiology of hepatocellular cancer (2)
cirrhosis
aflatoxin
aetiology of gall bladder cancer
galstone
porcelain GB
chronic typhoid infection
aetiology of cholangiocarcinoma
choledochal cyst
liver fluke
UC
primary sclerosing cholangitis
which has the highest suitable for surgery rate (hepatocellular carcinoma, gallbladder cancer or cholangiocarcinoma)
cholangiocarcinoma
example of primary liver cancer
hepatocellular carcinoma
gallbladder cancer cholangiocarcinoma
whats the most common secondary liver metastases
colorectal cancer
what’s the surgical resection aim in HCC
take away wherever lump is
and remove as little as possible
what’s the surgical resection aim in GB cancer
remove GB and the bits of liver the GB stuck to
what’s the surgical resection aim in cholangiocarcinoma
remove bile duct and bits the liver stuck to
what is the commonest form of pancreatic caner
pancreatic ductal adenocarcinoma
risk factors of pancreatic cancer
chronic pancreatitis
T2DM
cigarette smoking
diet, gall stones, past gastric surgery
FMH
gene that involves in hereditary pancreatitis
CFTR
PRSS1
SPINK1
gene involved in familial atypical multiple mole melanoma
CDKN2A
genes involved in familial breast ovarian cancer syndrome
BRAC1
BRAC2
PALB2
pathogenesis of pancreatic cancer
Pancreatic Intraepithelial Neoplasias (PanIN)
clinical presentations of carcinoma of head of pancreas
jaundice (due to invasion or compression of CBD)
weight loss (anorexia/ malabsorption)
pain
GI bleeding
pancreatitis
clinical presentation of carcinoma of body & tail of pancreas
vomiting (late stage due to DJ flexure)
weight loss with backpain
more advanced lesions than head of pancreas
is jaundice common in carcinoma of body & tail of pancreas
no
prognosis of carcinoma of body & tail of pancreas
mostly unresectable at the time of diagnosis
investigations of pancreatic cancer
tumor marker CA19-9 elevated
ultrasonography
dual-phase CT
MRI
MRCP
ERCP
endoscopic ultrasound
laparoscopy & laparoscopic US
PET
what can be identified using ultrasonography in pancreatic cancer
dilated bile ducts
pancreatic tumors
liver metastases
MRCP function in pancreatic cancer investigations
provides ductal images w/o complications of ERCP
ERCP function in pancreatic cancer investigations
confirms typical double duct sign
therapeutic modality for biliary stenting to relieve jaundice
aspiration of bile-duct system
function of endoscopic US in pancreatic cancer
detect small tumors
assess vascular invasion
fine needle aspiration
laparoscopy and laparoscopic US function in pancreatic cancer
detect occult metastatic lesions of liver and peritoneal cavity
PET function in pancreatic cancer
demonstrate occult metastases
where do neuroendocrine tumors arise from
gastroenteropancreatic tract
which genetic syndrome is commonly associated with neuroendocrine tumors
Multiple Endocrine Neoplasia Type 1 (MEN1)
biochemical investigations of NETs
chromogranin A (secreted by NETs)
gut hormones in fasting state
Calcium, PTH, prolactin, GH
24hr urinary 5-HIAA (serotonin metabolite)
imaging investigations of NETs
CT
MRI
bowel imaging (endoscopy, barium to follow, capsule endoscopy)
EUS
somatostatin receptor scintigraphy
treatments for NETs
curative resection (R0)
cytoreductive resection (R1/2)
liver transplant
medical, biotherapy, targeted therapy
what is GI cause of iron deficiency anaemia in order of frequency
aspirin/NSAIDs
colonic adnocarcinoma
gastric carcinoma
benign gastric ulcer
angiodyplasia
coeliac disease
gastrectomy
H.pylori
bowel ischaemia presentation
sudden onset crampy abdominal pain
bloody, loose stool
fever
pain on affected colon
which part does acute mesenteric ischaemia occurs
small bowel
which part does ischaemic colitis occur
large bowel
is acute mesenteric ischaemia occlusive and why
occulsive
due to thromboemboli
is ischaemic colitis occlusive or not
non-occlusive
low flow states or athersclerosis
does ischaemic colitis have acute or moderate pain
moderate pain and tenderness
bloods finding in bowel ischaemia (FBC and VBG)
FBC: neutrophilic leukocytosis
VBG: lactic acidosis
imaging findings in bowel ischaemia
disrupted flow
vascular stenosis
Pneomatosis intestinalis
thumbprint sign
bowel ischaemia investigations (3)
bloods
imaging (CT angiogram)
endoscopy
conservative management of bowel ischaemic colitis
IV fluid resuscitation
bowel rest
borad spectrum ABx
NG tube for decompression
anticoagulation
serial abdominal examination and repeat imaging
indications of bowel ischaemia
peritonitis or sepsis
massive bleeding
surgical management of bowel ischaemia
exploratory laparotomy
endovascular revascularisation
example of endovascular revascularisation for bowel ischaemia in patients without signs of ischaemia
balloon angioplasty
thrombectomy
what is mcburney’s point
tenderness in RLQ
test for appendix
what is blumberg sign
rebound tenderness in RIF
what is rovsing sign
RLQ pain on deep palpation of LLQ
test for appendicitis
what is psoas sign
RLQ pain on flexion of right hip against resistance
what is obturator sign
RLQ pain on passive internal rotation of hip with hip and knee flexion
blood results for acute appendicitis
FBC: neutrophilic leukocytosis
increased CRP
urinalysis
electrolyte imbalance due to vomiting
imaging tests for acute appendicitis
CT
USS
MRI
conservative management for acute appendicitis
IV fluids
analgesia
IV/PO antibiotics
what is interval appendicectomy
rate of recurrence after conservative management of abscess / perforation
2 surgical methods of acute appendicitis
open appendicectomy
laparoscopic
how to classify intestinal obstruction (3)
speed of onset (acute, chronic, acute-on-chronic)
site (high/low)
nature (simple/strangulating)
aetiology of bowel obstruction
lumen (faecal impaction, gallstone ileus)
wall (crohn’s disease, tumor, diverticulitis of colon)
outside wall (strangulated hernia, volvulus, obstruction due to adhesion)
aetiology of small bowel obstruction (4)
adhesion
neoplasia
incarcerated hernia
crohn’s
aetiology of large bowel obstruction (5)
colorectal carcinoma
volvulus
diverticulitis
faecal impaction
Hirschsprung disease
features that suggest strangulation in bowel
change in character of pain from colicky to continuous
tachycardia
pyrexia
peritonism
absent or reduced bowel sound
leucocytosis
increase CRP
imaging findings in SBO
erect CXR / AXR dilated small bowel loops >3cm proximal to obstruction
imaging findings in LBO
erect CXR / AXR dilated large bowel loops >6cm / caecum >9cm proximal to obstruction
CT abdo / pelvis imaging findings in bowel obstruction
transition point
dilation of proximal loops
IV +/- oral
AXR in SBO findings
ladder pattern of dilated loops at central position
striations pass completely across the width of distended loop produced by circular mucosal folds
AXR findings in LBO
distended peripherally
show haustrations of taenia coli
extend partially across whole width of bowel
benefits of doing CT for bowel obstruction (3)
localise site of obstruction
detect obstructing lesions and colonic tumors
can diagnose unusual hernia
supportive management for pt with bowel obstruction with no signs of ischaemia
NBM
IV peripheral access with large bore cannula
IV fluid resuscitation
analgesia
electrolyte baalnces
NG tube for decompression
urinary catheter
gradual food intake
conservative management for pt with bowel obstruction and faecal impaction
stool evacuation
conservative management for pt with bowel obstruction and sigmoid volvulus
rigid sigmoidoscopic decompression (use endoscope to detwisit bowel)
conservative management for pt with SBO
oral gastrograffin
what are indications of bowel obstructions to do surgery
haemodynamic instability
complete obstruction with signs of ischemia
closed loop obstruction
persistent bowel obstruction >2 days despite conservative management
operations examples for bowel obstruction
laparotomy
laparoscopy
restore intestinal transit
bowel resection with primary anastomosis
endoscopic stenting
presentation of GI perforation
sudden abdo pain with distention
diffuse abdominal guarding, rigidity, rebound tenderness
pain aggravated by movement
N+V
constipation
fever, tachycardia, tachypnoea, hypotension
decreased or no abdo sounds
4 kinds of perforation in GI
perforated peptic ulcer
perforated divierticulum
perforated appendix
perforated malignancy
presentations of perforated peptic ulcer (3)
sudden epigastric or diffuse pain
referred shoulder pain
Hx of NSAIDs, steroids, recurrent epigastric pain
presentations of perforated diverticulum (2)
LLQ pain
constipation
presentations of perforated appendix (3)
migratory pain
anorexia
gradual worsening RLQ pain
presentations of perforated malignancy (4)
change in bowel habit
weight loss
anorexia
rectal bleeding
blood findings in GI perofration
FBC: neutrophilic leukocytosis
elevated urea and creatinine
VBG: lactic acidosis
what will be seen in erect CXR in GI perforations
subdiaphragmatic free air
(pneumoperitoneum)
what will be seen in CT abdo/pelvis in GI perforations
pneumoperitoneum
free GI content
localised mesenteric fat stranding
supportive management on presentation for GI perforation
NBM
NG tube
IV peripheral access with large bore cannula
IV fluid resuscitation
broad spectrum Abx
IV PPI
parenteral analgesia and antiemetics
urinary catheter
consrevative management on presentation for GI perforation
abdo exam and imaging
IR-guided drainage of intra-abdominal collection
surgical management for GI perforation
exploratory laparoscopy/laparotomy
primary closure of perforation
resection of perforated segment
biliary colic symptoms (2)
postprandial RUQ pain with radiation to shoulder
nausea
investigation for biliary colic (bloods, USS)
normal bloods
USS: cholelithiasis
management for biliary colic
analgesia
antiemetics
follow up for elective cholecystectomy
acute cholecystitis symptoms (3)
acute, severe RUQ pain
fever
murphy’s sign
acute cholecystitis investigation findings (bloods, USS)
blood: elevated WBC/CRP
USS: thickened gallbladder wall
management for acute cholecystitis
fluids
Abx
analgesia
blood culture
early or elective cholecystectomy
acute cholangitis symptoms (3)
charcot’s triad (jaundice, RUQ pain,fever)
acute cholangitis investigation findings (bloods, USS)
blood: elevated WBC, CRP, LFT,blood MCS +ve
USS: biliary dilation
acute cholangitis management
fluids
IV Abx
analgesia
ERCP for clearance of bile duct or stenting
acute pancreatitis symptoms (3)
severe epigastric pain radiate to back
Nausea +/- vomit
Hx of gallstones or EtOH use
acute pancreatitis investigation findings (bloods, CT+USS)
raised amylase/lipase
high WBC, low Ca2+
CT+USS to assess for complications or causes
acute pancreatitis management
scoring (glasgow-imrie)
fluid resuscitation, O2, analgesia, antiemetics
ITU/HDU involvement
which obstruction usually accompanied by early and profuse vomiting, large or small bowel?
SBO
conservative management in sigmoid volvulus
sigmoidoscope
use a large well lubricated, soft rubber rectal tube to pass along the sigmoidoscope
this untwists the volvulus and release many flatus and liquid faeces
risk of untreated volvulus
torsion cut off blood supply
necrosis of the area
what is Hartmann’s procedure
removing a section of the large bowel
exploratory laparotomy & Sigmoid colectomy with end colostomy
how to restore blood flow in SMA (3)
embolectomy in acute mesenteric ischaemia
endovascular management of SMA in thrombus acute mesenteric ischaemia
arterial bypass of SMA in thrombotic AMI
what are 4 kinds of acute mesenteric ischaemia
- embolism (50%)
- thrombosis (20-35%)
- nonocclusive (<5%)
- Venous (10-15%)
what is portal pyaemia (pylephlebitis)
septic thrombophlebitis of portal venous system
complications of portal pyaemia
diverticulitis
appendicitis
