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

Gastro - Upper GI tract Flashcards

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
Q

What are typical symptoms of reflux

A

Heartburn
Chest pain
Resurgence
Sensitivity to foods - cold in particular (water)
Acid brash
Worse with leaning forwards
Worse at night

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26
Q

What are some asymptomatic symptoms of reflux

A

Cough
Dental issues
Throat clearing
Ears - ache sinusitis, Otis media
Sleep - apnoea, disturbance,
Pulmonary - asthma, fibrosis etc

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27
Q

Why do you have to take tablet 30 to 40 mins before eating

A

So the tablet is absorbed and working before you take food

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28
Q

What are some red flag symptoms of GORD

A

Weight loss
Anaemia
Dysphasia

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29
Q

What are the 2 phenotypes of GORD

A

Non erosive
Erosive
Barrets

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30
Q

What are 2 types of functional oesophageal disorders

A

Reflux hypersensitivity
Functional heartburn

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31
Q

What are some complications of reflux

A

Erosive oesophagitis
Aspiration
Barrets oesophagus
Peptic stricture

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32
Q

What is the line between the stomach and oesophagus

A

Z line

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33
Q

What is the treatment for reflux

A

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

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34
Q

what are the 2 main types of oesophageal cancer

A

adenocarcimona - most common in the west
squamous cell carcinoma - 90%

35
Q

what does the oesophagus not have

A

a surosa

36
Q

SCC of oesophagous where is it most common

A

asian oesophageal cancer belt

37
Q

what is the main risk factor of squamous cell carcinoma

A

cigarette smoking
alcohol
previous head and neck cancer
radiotherapy

38
Q

what is adenocarcinoma associated with

A

GORD

39
Q

what is the alarm symptoms of cancer

A

progressive dysphagia
Change to liquid diet
Weight loss
Regurgitation
Persistent reflux NOT responding to PPI
Others e.g., food bolus obstruction

40
Q

what is the curative pathway

A

4 cycles of chemotherapy – eradicate systemic disease, prevent disease progression
Surgery
Adjuvant chemo = 4 further cycles of chemotherapy (75% dose)

41
Q

what is the chemo used

A

FLOT4
over ECX

42
Q

why is radiotherapy given for squamous cell cancers

A

squamous cell cancers are very sensitive to radiotherapy

43
Q

what is the only blood vessel that stays after surgery

A

right gastroepiploic

44
Q

how does gastric cancer present

A

Iron deficiency anaemia
Early satiety
Weight loss
Abdominal pain / mass
Reflux
Non healing gastric ulcer

45
Q

what bacteria can cause gastric cancer

A

H pylori

46
Q

what are some emergency symptoms of gastric cancer

A

Disseminated ascites
Haematemesis / Melaena i.e., upper GI bleed
Gastric outlet obstruction
Perforated gastric ulcer

47
Q

which are correct answers regarding the ligament of treitz

A

a

48
Q

which species always cause infetion

A

Strep pyrogenes N
Neisseria sp N
Treponema pallidum Y
Chlamydia trachomatis
Y
Streptococcal milleri N

49
Q

number 1 acuse of sore throat is strep pyogenes

A

False - viruses

50
Q

sore throat and fever always needs antibiotics

A

False - viral

51
Q

H pylori associated with MALT

A

True

52
Q

EBV causes infective mononeucleois

A

True

53
Q

normal oropharyngeal bacteria

A

“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
Q

most common oral microflora

A

s mutans

55
Q

what is dental plaque made of

A

streptococci

56
Q

how common is colorectal cancer

A

VERY common
42,042 new cases per year UK
also high mortality
> 20% pts present with distant metastasis

57
Q

where is colorectal cancer most common

A

in europe and north america
(prostate and breast cancer have similar distribution)

58
Q

what age and sex is colorectal cancer most common

A

85-89yrs
men slightly more than women

59
Q

what are the risk factors for colorectal cancer

A

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
Q

what is FAP

A

Familial Adenomatous Polyposis

61
Q

is FAP dominant or recessive

A

dominant - APC gene on chromosome 5q (tumor suppressor gene)

62
Q

what do you see in FAP

A

hundreds of adenomatous polyps
risk of developing colorectal cancer exceeds 90% by age 70 years without surgery

63
Q

what is the manamgnet of FAP

A

Prophylactic surgery 16-25 years depending on polyp count / size / dysplasia and social factors

64
Q

what is HNPCC

A

Hereditary Non-Polyposis Colorectal Cancer

65
Q

is it dominant or recessive

A

dominant - DNA mismatch

66
Q

what is the management for patients with HNPCC

A

colonoscopy screening every 2 years

67
Q

what percentage of colorectal cancers are due to FAP and HNPCC

A

20%

68
Q

what are some of the mutations that are asociated with cancers

A

ACP / CTNNB1 / AXIN1 / hMLH1 / hMSH2

69
Q

where in the bowel is cancer most common

A

rectum
sigmoid colon
caecum

70
Q

what clinical features would someone present with if they had colorectal cancer

A

Change in bowel habit
Rectal bleeding
Anaemia
Abdominal pain
Mucus / tenesmus
Abdominal mass
Weight loss
Emergency – approx 25% - obstruction, peritonitis, bleeding

71
Q

how is someone with suspected colorectal cancer evaluated

A

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
Q

why would you do colonic stenting

A

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
Q

what are complications of surgery

A

Anastomotic leak
Wound infection
DVT / PE
Bleeding
Nerve injury
Cardiopulmonary
Stoma complications

74
Q

when do you consider an anastomosis leak and what blood tests would you do

A

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
Q

what staging is used in colorectal cancer

A

Dukes staging (A-D)
and TNM

76
Q

what does pT1 to pT4b mean. which layers are being invaded

A

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
Q

what does pN0 to pN2b mean

A

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
Q

what does metastisis staging pM1a to pM1c mean

A

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
Q

what are the 3 types of chemotherapy

A

Neo-adjuvant
Adjuvant
Palliative

80
Q

when do you use adjucant chemotherapy

A

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
Q

which is more common colorectal or anal cancer

A

colorectal
400 poeple died of anal cancer from 2015-2017

82
Q

anal cancer is more common in men (T or F)

A

F
more common in women
18:10

83
Q

what is the main risk factor for anal cancer

A

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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