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MBBS - Year 3 > Gastro - Upper GI tract > Flashcards

Gastro - Upper GI tract Flashcards

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1
Q

How much HCl does the stomach make daily

A

1.5L of HCl

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2
Q

What is gastro-oesophageal reflux disease

A

Imbalance between damaging and protecting
Acid, pepsin, bile
Oesophageal clearance and sphincter function

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3
Q

How do antacids work

A

Neutralise gastric acid
Rapid onset
Large doses heal duodenal ulcers
Symptomatic relief (GORD, indigestion)

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4
Q

What are common antacids

A

Magnesium - diarrhoea, calcium, sodium or aluminium - constipation, containing tablets or liquid

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5
Q

What are adverse effects of antacids

A

Milk-alkali syndrome
Chronic renal failure
Belching - release of CO2
Ca stimulates gastrin - counter productive
Many are high in Na

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6
Q

What is aligning acid

A

Gaviscon
Floats on gastric contents
Protects against oesophageal reflux
Can be combined with antacids

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7
Q

What are examples of H2 receptor antagonists

A

Cimetidine
Ranitidine - removed
Nizatidine
Famotidine
Reversible competitive antagonists
(Parietal cells and cardiac atria)

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8
Q

How do H2 receptor antagonists work

A

Reduce nasal and stimulated acid secreted
Reduce pepsin secretion by about 60%
Rate of ulcer healing dependent on degree of acid suppression

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9
Q

H2 pharmacokinetics

A

Short half life
Cimetidine really excreted
Other renal and metabolism excretion

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10
Q

What are H2 antagonist side effects

A

Diarrhoea
Headache
Confusion in elderly
Cimetidine - antiandrogen - gynaecomastia
Cimetidine - inhibits P450 - enhances warfarin, theophylline, toldutamide

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11
Q

What are some examples of proton pump inhibitors

A

Irreversible inhibition of H secretion
Omeprazole
Lansoprasole
Esomeprazole
Rabeprazole
Pantoprazole

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12
Q

How do proton pumps inhibitors work

A

Inhibit acid secretion by 90%
Covalently inhibit PP
Recovery requires new synthesis
Serum levels unrelated to action

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13
Q

What is omeprazole and how does it work

A

Prodrug, unstable in acid
Enteric coated
Concentrated and pronated in parietal cell
Absorbed in small bowel

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14
Q

How are PPI metabolised

A

All via P450 system
CYP2C19 activity genetically predetermined - fast metabolisers common in white pop
- slow metabolisers common in Asian pop

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15
Q

What are side effects of PPIs

A

Diarrhoea
Headache
Infectious gastroenteritis
Impaired calcium and magnesium absorption
Hypergastrinaemia and acid rebnound

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16
Q

Why do we make gastric acid

A

Kill pathogens
NOT digest food

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17
Q

What is acid suppression used for

A

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

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18
Q

GORD which treatment best

A

PPI better than H2 receptor blockers

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19
Q

What is misoprostol and how does it work

A

PGE1 analogue
EP3 agonist
Inhibits acid secretion
Increases duodenal bicarbonate secretion\increases gastric mucus production
Increases mucosal blood flow
Gastroprotection

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20
Q

What are some of the side effects

A

Have to take 4x a day
Diarrhoea 30%
Uterine contractions
Menorrhagia and post-menopausal bleeding

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21
Q

What is a basic background of gastrooesophageal reflux disease

A

Largest worldwide expenditure
Very common
Common in kids - failure to thrive

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22
Q

What is the antireflux barrier

A

Lower oesophageal sphincter (LES) and gastroeosophageal junction (GEJ) and diaphragm, crura - MOST IMPORTSNT

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23
Q

What happens if crura is below the oesophagus

A

Hiatus hernia - very common for reflux

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24
Q

What are the different types of hiatus hernia

A

Sliding - MOST common
Small - <2
Large - >5

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25
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
26
What are some asymptomatic symptoms of reflux
Cough Dental issues Throat clearing Ears - ache sinusitis, Otis media Sleep - apnoea, disturbance, Pulmonary - asthma, fibrosis etc
27
Why do you have to take tablet 30 to 40 mins before eating
So the tablet is absorbed and working before you take food
28
What are some red flag symptoms of GORD
Weight loss Anaemia Dysphasia
29
What are the 2 phenotypes of GORD
Non erosive Erosive Barrets
30
What are 2 types of functional oesophageal disorders
Reflux hypersensitivity Functional heartburn
31
What are some complications of reflux
Erosive oesophagitis Aspiration Barrets oesophagus Peptic stricture
32
What is the line between the stomach and oesophagus
Z line
33
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
34
what are the 2 main types of oesophageal cancer
adenocarcimona - most common in the west squamous cell carcinoma - 90%
35
what does the oesophagus not have
a surosa
36
SCC of oesophagous where is it most common
asian oesophageal cancer belt
37
what is the main risk factor of squamous cell carcinoma
cigarette smoking alcohol previous head and neck cancer radiotherapy
38
what is adenocarcinoma associated with
GORD
39
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
40
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)
41
what is the chemo used
FLOT4 over ECX
42
why is radiotherapy given for squamous cell cancers
squamous cell cancers are very sensitive to radiotherapy
43
what is the only blood vessel that stays after surgery
right gastroepiploic
44
how does gastric cancer present
Iron deficiency anaemia Early satiety Weight loss Abdominal pain / mass Reflux Non healing gastric ulcer
45
what bacteria can cause gastric cancer
H pylori
46
what are some emergency symptoms of gastric cancer
Disseminated ascites Haematemesis / Melaena i.e., upper GI bleed Gastric outlet obstruction Perforated gastric ulcer
47
which are correct answers regarding the ligament of treitz
a
48
which species always cause infetion
Strep pyrogenes N Neisseria sp N Treponema pallidum Y Chlamydia trachomatis Y Streptococcal milleri N
49
number 1 acuse of sore throat is strep pyogenes
False - viruses
50
sore throat and fever always needs antibiotics
False - viral
51
H pylori associated with MALT
True
52
EBV causes infective mononeucleois
True
53
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)
54
most common oral microflora
s mutans
55
what is dental plaque made of
streptococci
56
how common is colorectal cancer
VERY common 42,042 new cases per year UK also high mortality > 20% pts present with distant metastasis
57
where is colorectal cancer most common
in europe and north america (prostate and breast cancer have similar distribution)
58
what age and sex is colorectal cancer most common
85-89yrs men slightly more than women
59
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
60
what is FAP
Familial Adenomatous Polyposis
61
is FAP dominant or recessive
dominant - APC gene on chromosome 5q (tumor suppressor gene)
62
what do you see in FAP
hundreds of adenomatous polyps risk of developing colorectal cancer exceeds 90% by age 70 years without surgery
63
what is the manamgnet of FAP
Prophylactic surgery 16-25 years depending on polyp count / size / dysplasia and social factors
64
what is HNPCC
Hereditary Non-Polyposis Colorectal Cancer
65
is it dominant or recessive
dominant - DNA mismatch
66
what is the management for patients with HNPCC
colonoscopy screening every 2 years
67
what percentage of colorectal cancers are due to FAP and HNPCC
20%
68
what are some of the mutations that are asociated with cancers
ACP / CTNNB1 / AXIN1 / hMLH1 / hMSH2
69
where in the bowel is cancer most common
rectum sigmoid colon caecum
70
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
71
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
72
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
73
what are complications of surgery
Anastomotic leak Wound infection DVT / PE Bleeding Nerve injury Cardiopulmonary Stoma complications
74
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
75
what staging is used in colorectal cancer
Dukes staging (A-D) and TNM
76
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)
77
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
78
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
79
what are the 3 types of chemotherapy
Neo-adjuvant Adjuvant Palliative
80
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
81
which is more common colorectal or anal cancer
colorectal 400 poeple died of anal cancer from 2015-2017
82
anal cancer is more common in men (T or F)
F more common in women 18:10
83
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

MBBS - Year 3 (13 decks)

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