Gastro - Upper GI tract Flashcards
How much HCl does the stomach make daily
1.5L of HCl
What is gastro-oesophageal reflux disease
Imbalance between damaging and protecting
Acid, pepsin, bile
Oesophageal clearance and sphincter function
How do antacids work
Neutralise gastric acid
Rapid onset
Large doses heal duodenal ulcers
Symptomatic relief (GORD, indigestion)
What are common antacids
Magnesium - diarrhoea, calcium, sodium or aluminium - constipation, containing tablets or liquid
What are adverse effects of antacids
Milk-alkali syndrome
Chronic renal failure
Belching - release of CO2
Ca stimulates gastrin - counter productive
Many are high in Na
What is aligning acid
Gaviscon
Floats on gastric contents
Protects against oesophageal reflux
Can be combined with antacids
What are examples of H2 receptor antagonists
Cimetidine
Ranitidine - removed
Nizatidine
Famotidine
Reversible competitive antagonists
(Parietal cells and cardiac atria)
How do H2 receptor antagonists work
Reduce nasal and stimulated acid secreted
Reduce pepsin secretion by about 60%
Rate of ulcer healing dependent on degree of acid suppression
H2 pharmacokinetics
Short half life
Cimetidine really excreted
Other renal and metabolism excretion
What are H2 antagonist side effects
Diarrhoea
Headache
Confusion in elderly
Cimetidine - antiandrogen - gynaecomastia
Cimetidine - inhibits P450 - enhances warfarin, theophylline, toldutamide
What are some examples of proton pump inhibitors
Irreversible inhibition of H secretion
Omeprazole
Lansoprasole
Esomeprazole
Rabeprazole
Pantoprazole
How do proton pumps inhibitors work
Inhibit acid secretion by 90%
Covalently inhibit PP
Recovery requires new synthesis
Serum levels unrelated to action
What is omeprazole and how does it work
Prodrug, unstable in acid
Enteric coated
Concentrated and pronated in parietal cell
Absorbed in small bowel
How are PPI metabolised
All via P450 system
CYP2C19 activity genetically predetermined - fast metabolisers common in white pop
- slow metabolisers common in Asian pop
What are side effects of PPIs
Diarrhoea
Headache
Infectious gastroenteritis
Impaired calcium and magnesium absorption
Hypergastrinaemia and acid rebnound
Why do we make gastric acid
Kill pathogens
NOT digest food
What is acid suppression used for
GORD
Healing peptic ulcers
Prevent NSAID induced peptic ulcer
H. Pylori eradication
Stress ulcer (ITU - ischaemia of gut) and aspiration prevention
Non-responsive Zollinger-Ellison syndrome
GORD which treatment best
PPI better than H2 receptor blockers
What is misoprostol and how does it work
PGE1 analogue
EP3 agonist
Inhibits acid secretion
Increases duodenal bicarbonate secretion\increases gastric mucus production
Increases mucosal blood flow
Gastroprotection
What are some of the side effects
Have to take 4x a day
Diarrhoea 30%
Uterine contractions
Menorrhagia and post-menopausal bleeding
What is a basic background of gastrooesophageal reflux disease
Largest worldwide expenditure
Very common
Common in kids - failure to thrive
What is the antireflux barrier
Lower oesophageal sphincter (LES) and gastroeosophageal junction (GEJ) and diaphragm, crura - MOST IMPORTSNT
What happens if crura is below the oesophagus
Hiatus hernia - very common for reflux
What are the different types of hiatus hernia
Sliding - MOST common
Small - <2
Large - >5
What are typical symptoms of reflux
Heartburn
Chest pain
Resurgence
Sensitivity to foods - cold in particular (water)
Acid brash
Worse with leaning forwards
Worse at night
What are some asymptomatic symptoms of reflux
Cough
Dental issues
Throat clearing
Ears - ache sinusitis, Otis media
Sleep - apnoea, disturbance,
Pulmonary - asthma, fibrosis etc
Why do you have to take tablet 30 to 40 mins before eating
So the tablet is absorbed and working before you take food
What are some red flag symptoms of GORD
Weight loss
Anaemia
Dysphasia
What are the 2 phenotypes of GORD
Non erosive
Erosive
Barrets
What are 2 types of functional oesophageal disorders
Reflux hypersensitivity
Functional heartburn
What are some complications of reflux
Erosive oesophagitis
Aspiration
Barrets oesophagus
Peptic stricture
What is the line between the stomach and oesophagus
Z line
What is the treatment for reflux
Lifestyle changes - weight loss, stop smoking, diet, caffeine, eat 3 hours before bed, stress
Pharmacological - PPI, H2 antagonists, Baclofen and Amitryptiline, antacids
Surgery - Nissan fundoplication surgery
what are the 2 main types of oesophageal cancer
adenocarcimona - most common in the west
squamous cell carcinoma - 90%
what does the oesophagus not have
a surosa
SCC of oesophagous where is it most common
asian oesophageal cancer belt
what is the main risk factor of squamous cell carcinoma
cigarette smoking
alcohol
previous head and neck cancer
radiotherapy
what is adenocarcinoma associated with
GORD
what is the alarm symptoms of cancer
progressive dysphagia
Change to liquid diet
Weight loss
Regurgitation
Persistent reflux NOT responding to PPI
Others e.g., food bolus obstruction
what is the curative pathway
4 cycles of chemotherapy – eradicate systemic disease, prevent disease progression
Surgery
Adjuvant chemo = 4 further cycles of chemotherapy (75% dose)
what is the chemo used
FLOT4
over ECX
why is radiotherapy given for squamous cell cancers
squamous cell cancers are very sensitive to radiotherapy
what is the only blood vessel that stays after surgery
right gastroepiploic
how does gastric cancer present
Iron deficiency anaemia
Early satiety
Weight loss
Abdominal pain / mass
Reflux
Non healing gastric ulcer
what bacteria can cause gastric cancer
H pylori
what are some emergency symptoms of gastric cancer
Disseminated ascites
Haematemesis / Melaena i.e., upper GI bleed
Gastric outlet obstruction
Perforated gastric ulcer
which are correct answers regarding the ligament of treitz
a
which species always cause infetion
Strep pyrogenes N
Neisseria sp N
Treponema pallidum Y
Chlamydia trachomatis
Y
Streptococcal milleri N
number 1 acuse of sore throat is strep pyogenes
False - viruses
sore throat and fever always needs antibiotics
False - viral
H pylori associated with MALT
True
EBV causes infective mononeucleois
True
normal oropharyngeal bacteria
“Viridans” Streptococci
Streptococcus ‘milleri’
S.pyogenes (Group A Strep) (asymptomatic carriers)
Diphtheroids
Coagulase negative staphylococci
Staphylococcus aureus (4-64 % carrier)
Moraxella/Neisseria/Haemophilus spp.
Anaerobes
Gram negatives, anaerobic streptococci
HSV, EBV, CMV (latent virus shedding)
most common oral microflora
s mutans
what is dental plaque made of
streptococci
how common is colorectal cancer
VERY common
42,042 new cases per year UK
also high mortality
> 20% pts present with distant metastasis
where is colorectal cancer most common
in europe and north america
(prostate and breast cancer have similar distribution)
what age and sex is colorectal cancer most common
85-89yrs
men slightly more than women
what are the risk factors for colorectal cancer
Age
Genetic syndromes
Diet: high in fat and cholesterol - processed food
Obesity: 30% increase if BMI > 30
Alcohol: 33% increase > 6 units per day
Diabetes: 22-30% higher in people with type II diabetes, compared with non-diabetics
Smokers: 17-21% higher in current smokers
what is FAP
Familial Adenomatous Polyposis
is FAP dominant or recessive
dominant - APC gene on chromosome 5q (tumor suppressor gene)
what do you see in FAP
hundreds of adenomatous polyps
risk of developing colorectal cancer exceeds 90% by age 70 years without surgery
what is the manamgnet of FAP
Prophylactic surgery 16-25 years depending on polyp count / size / dysplasia and social factors
what is HNPCC
Hereditary Non-Polyposis Colorectal Cancer
is it dominant or recessive
dominant - DNA mismatch
what is the management for patients with HNPCC
colonoscopy screening every 2 years
what percentage of colorectal cancers are due to FAP and HNPCC
20%
what are some of the mutations that are asociated with cancers
ACP / CTNNB1 / AXIN1 / hMLH1 / hMSH2
where in the bowel is cancer most common
rectum
sigmoid colon
caecum
what clinical features would someone present with if they had colorectal cancer
Change in bowel habit
Rectal bleeding
Anaemia
Abdominal pain
Mucus / tenesmus
Abdominal mass
Weight loss
Emergency – approx 25% - obstruction, peritonitis, bleeding
how is someone with suspected colorectal cancer evaluated
History & examination
Digital examination
Sigmoidoscopy / proctoscopy
Examination of colon – colonoscopy
Staging examination – CT / U/S / MRI
Blood investigations - CEA
Assessment of fitness for treatment
why would you do colonic stenting
Initially used in patients with metastatic disease
Used in large bowel obstruction to get patient fit and plan elective surgery
Occasionally in benign strictures
what are complications of surgery
Anastomotic leak
Wound infection
DVT / PE
Bleeding
Nerve injury
Cardiopulmonary
Stoma complications
when do you consider an anastomosis leak and what blood tests would you do
Any deterioration in condition within 10 days
Elderly – often present with cardiac / respiratory symptom – e.g. AF
Difficult to diagnose if epidural still running
Even consider in presence of defunctioning stoma
Raised CRP, WCC, metabolic acidosis
If detected early - reduced morbidity
Needs to be excluded – CT with contrast
what staging is used in colorectal cancer
Dukes staging (A-D)
and TNM
what does pT1 to pT4b mean. which layers are being invaded
pT1 Tumour invades submucosa
pT2 Tumour invades muscularis propria
pT3 Tumour invades into subserosa or into non-peritonealised pericolic or perirectal tissues
pT4 Tumour perforates visceral peritoneum (4a) and/or directly invades other organs or structures (4b)
what does pN0 to pN2b mean
pN0 – No lymph node metastatic disease
pN1 - 1–3 regional lymph nodes
pN1a - 1 regional lymph node
pN1b - 2–3 regional lymph nodes
pN1c - Tumour deposit(s) in the subserosa,
pN2 - 4 or more regional lymph nodes
pN2a - 4–6 regional lymph nodes
pN2b - Metastases in 7 or more lymph nodes
what does metastisis staging pM1a to pM1c mean
pM1a Metastasis confined to one organ without peritoneal metastases
pM1b Metastases in more than one organ
pM1c Metastases to the peritoneum with or without other organ involvement
what are the 3 types of chemotherapy
Neo-adjuvant
Adjuvant
Palliative
when do you use adjucant chemotherapy
Early stage tumours, no nodal disease, no risk factors
not needed
No nodal disease, two risk factors on MDT
recommended if fit
Node positive
recommended if fit
which is more common colorectal or anal cancer
colorectal
400 poeple died of anal cancer from 2015-2017
anal cancer is more common in men (T or F)
F
more common in women
18:10
what is the main risk factor for anal cancer
HPV – type 16 / 18
Around 91% of anal cancers in women and 75% in men are HPV-positive
Smoking / lowered immunity HIV
Hx cervical cancer / large no. sexual partners
