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Gastro > Upper GI > Flashcards

Upper GI Flashcards

1
Q

Diagnosis of GORD

A

Made on symptoms alone

Response to acid suppression

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2
Q

Management of GORD

A 
Weight loss
Stop smoking
Decrease ETOH, coffee, chocolate, spicy, fatty food
Avoid late meals
Elevate head of bed
Above effective only 20-30%

PPI >H2 antagonist (80 vs 50% efficacy)

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3
Q

What’s barrett’s?
What causes it?
Classification

A

Intestinal metaplasia of the distal oesophageal mucosa (to columnar mucosa)

Begins at LOS and extends variable distances (can be circumferential or tongues)

Correlates with severity of reflux
Needs 10 years of reflux (often silent)
15% with reflux oesophagitis

Classification
Short vs long segment (<3cm vs >3cm)
Long segment = increased risk of malignancy

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4
Q

Rx Barrett’s - high grade dysplasia on endoscopy

A

PPI
Endoscopic ablation therapy
Much less mortality now

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5
Q

Rx Barrett’s - no dysplasia

A

PPI - limited data that it reduces chance of dysplasia

Surveillance endoscopy 6 months –> 3 years

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6
Q

Rx Barrett’s - low grade dysplasia

A

PPI

Repeat endoscopy 6 months

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7
Q

Rings down a oesophagus
Recurrent dysphagia
What is it?

A

Eosinophil oesophagitis

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8
Q

What is Eosinophil oesophagitis?

A

Chronic immune mediated inflammatory disease of the oesophagus

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9
Q

Presentation of eosinophil oesophagitis

A

Dysphagia, food impaction
Young males
Associated with asthma, atopy

Endoscopy - rings and furrows, tears on dilation
Histology: eosinophil infiltration (proximal and mid oesophagus; eosinophils can be seen in distal oesophagus in GORD)

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10
Q

Rx eosinophil oesophagitis

A

PPI (85% effective)

2nd line: topical steroids (fluticasone puffer or budesonide slurry)

Elimination diets work well in children (not really in adults - we think its more to do with the air you breathe in)

Oesophageal dilatation if strictures

Last line: oral steroids (budesonide) +/- azathioprine +/- dupilimumab (monoclonal Ab IL4 IL13)

Dupilimumab is recently approved for use

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11
Q

What’s achlalasia?

A

Incomplete LOS relaxation

Aperistalsis

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12
Q

Presentation of aclalsia

A

Dysphagia to solids and liquids
Regurgitation especially postural (night), saliva and old food (not acid)
weight loss
Chest discomfort/pain (may mimic heartburn)
aspiration

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13
Q

Investigation achlasia

A

Endoscopy

  • Dilated oesophagus, tight LOS, food in oesophagus
  • Done to exclude strictures

Barium swallow - birds beak

Manometry

  • Most sensitive
  • Incomplete LOS relaxation
  • Aperistalsis
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14
Q

Rx achlasia

A

1) Nitrates or CCB
- Generally not effective as the doses that need to be used have large effects on BP

Definitive treatment
2) BOTOX reserved for old patients or too unwell for other definitive therapy

3) Per oral endoscopic myotomy (POEM) is 1st line
- high response, low mortality

4) Balloon dilatation of LOS - 2nd line
- Done in 15-20 minutes
- High response rate
- Low perforation rate
- Not as longstanding as POEM, often requires repetition

5) Laparoscopic hellers myotomy - 3rd line
- Still a role
- Complex operation
- High mortality
- Good response

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15
Q

What are varices?

A

Venous collaterals which form in the presence of portal HTN
Hepatic venous pressure gradient (HVPG) of >12mmHg required for formation
HVPG usually >18mmHg before bleed

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16
Q

Rx varices

A

Endoscopy every 6-12 months (usually at diagnosis of cirrhosis/portal HTN)

If no varices - repeat 12 months

If large varices - B blocker (propanolol, carvediolol)
- Need to reduce the resting pulse by 25% for it to be effective

If grade 2-3 varices - banding

No difference in mortality between B blocker and banding

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17
Q

Rx variceal haemorrhage

A

Non-aggressive resuscitation. Aim Hb >70.

1) Ceftriaxone, followed by norfloxacin (7 days)
- reduce mortality, rebleeding rate, infection
- bacteria goes straight from azygous vein to vascular supply/Rt heart

2) endoscopy + banding
- Within 12 hours
- Gastric varices: glue injection preferred

3) Terlipressin or octreotide
- Acute
- Usually used for 3-5 days
- CI IHD, vascular disease

4) Sengstaken-Blakemore or linton tube
- Temporary measure (24-48h) due to risk of pressure necrosis. Use only if banding fails and you need to quickly stop bleeding.
- Insert it like an NGT and inflate the balloon to compress haemorhaging varices in oesophagus and stomach

5) Danis stent (bridge to TIPSS or surgical implantation)
- For those who fail endoscopic therapy, usually due to previous band induced scarring. Varix doesn’t suck up the band.
- Tamponades the bleed
- Superior to Sengstaken tube in small case series

6) TIPSS
- CI in encephalopathy, portal vein thrombosis
- Best thing to do if ongoing bleeding after banding but technically challenging

+/- PPI doesn’t change immediately but may reduce risk of post-banding ulcers

Don’t use erythromycin

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18
Q

Risk factors PUD

A 
H pylori
NSAIDs
Smoking
Stress - ICU/comorbid
Chemo agents
Crohn's 
Gastrinoma (Zollinger-Ellison syndrome)
Immunosuppression like steroids - prevents healing of small lesions, doesn't cause ulcers
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19
Q

Repeat positive urea breath test after treatment for h pylori (amoxycillin + clarithromycin + PPI)
What to do?

A

Clarithryomycin resistance >10% resistance

If resistant…
1st line: Rifabutin, doxycyline/tetracycline, PPI, amoxycillin
2nd line: levofloxacin (salvage therapy)

Others
Bismuth containing quadruple therapy (not used much anymore)
Culture and sensitivity

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20
Q

Rx H pylori

A

1st line
amox (<10% resistance), clarithromycin, PPI

Penicillin allergy
Clarithromycin, metronidazole (>30% resistance), PPI

HIgh resistance
Amoxycillin, metronidazole, PPI

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21
Q

Relative NSAID toxicity in terms of PUD

A

Aspirin >Indomethacin > ibuprofen >diclofenac > COX2 inhibitor

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22
Q

Rx gastric ulcer

A

Gastric ulcers can be malignancy
Duodenal ulcers are very rare

Repeat endoscopy in 8 weeks
PPI

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23
Q

Rx PUD

A

Treat H pylori
Modify NSAID - change aspirin to clopidogrel
PPI

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24
Q

How long does a gastric ulcer take to heal?

A

8 weeks

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25
Q

How much blood to get melena?

A

150ml

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26
Q

Red PR bleeding from an upper GI soruce. how much?

A

Varices and duodenal ulcers

>500ml

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27
Q

Bleeding duodenal ulcer Rx

A

Inject with adrenaline

Heat probe

Vascular clip

Sprays

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28
Q

What’s a classification for ulcers?

A

Forrest classification of ulcers
High risk of recurrence: Active bleeding, clot, vessel - high risk of bleeding

Low risk ulcers - clean base, flat red spot

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29
Q

Rx high risk ulcer

A

PPI infusion for 72h after endoscopic therapy (from time of gastroscopy, not from presentation)
- Reduces rebleeding rate, improves mortality

Must be infusion - changes pH in stomach, stops acid from dissolving clot

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30
Q

Can Barrett’s extend overtime?

A

Yes if they don’t take PPI
But in general it doesn’t if you take PPI
Short segments can regress after 5-10 years PPI

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31
Q

Pathophysiology of coeliac

A

1) environmental
- Gluten

2) genetic
- HLADQ2 or DQ8

3) immunological
- TTG deaminates gliadin to peptides to presentation by APC to CD4 T cells

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32
Q

Clinical features of coeliac

A

Diarrhoea +/- abdo pain/discomfort (<50% cases)

Others

  • OP
  • IDA
  • Infertility and recurrent miscarriages
  • Weight loss
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33
Q

Diagnosis of coeliac

  • Serology
  • Small bowel biopsy
  • HLA typing
A

tTG-IgA + Total IgA level
Reason we do total IgA is because 2% of coeliac disease is IgA deficient

Other option is tTG-IgA + DGP-IgG

Serology cannot diagnose Coeliac in isolation.
High risk patients with negative serology should have small bowel biopsy.

Small bowel biopsy (gold standard)

  • Villous atrophy with crypt hyperplasia, raised intraepithelial lymphocytes
  • Biopsy from the 1st (x2) and 2nd (x4) part of duodenum
  • If any doubt, do 2 week gluten challenge then rebiopsy

HLA typing

  • Excellent NPV but poor PPV
  • Does not depend on gluten intake
  • Absence of HLADA2.5, DQ2.2 and DQ8 exclude the diagnosis
  • Presence of HLADQ2 or DQ8 indicates susceptibility to disease but doesn’t mean they have coeliac
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34
Q

Management of coeliac

A

Gluten free diet
- Recovery takes 6 months+

Refractory disease: may respond to corticosteroids

Nutritional assessment: Fe deficiency, folate, B12, Vitamin D, hypocalcaemia, magnesium, zinc

Screen for complications: TSH, LFTs, fasting BSL, DEXA

Vaccinations (higher risk for pneumococcal sepsis due to hyposplenism)

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35
Q

Associations with coeliac

A

autoimmune thyroiditis (Hashimoto or Grave’s) (5% have coeliac)
T1DM
Down’s
Dermatitis herpetiformis (50% will have coeliac)
Recurrent infertility (will return to normal after GFD), miscarriages at 8/52 (coeliac ab cross placenta and will attack foetus)
Osteoporosis and fractures (chronic inflammation; poor vitamin D, calcium absorption)
Ataxia, epilepsy

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36
Q

Coeliac disease for 40 years
Sudden weight loss and diarrhoea
What do you do?

A

High risk of small bowel T cell lymphoma (6th decade) or small bowel adenocarcinoma

Do CT abdo pelvis

37
Q

Why is a gluten free diet important in coeliac?

A

Reduces adenocarcinoma
Reduces BMD loss and fractures
Improves fertility
Improves mortality

Unfortunately has no effect on T cell lymphoma

38
Q

Refractory coeliac disease

A

1% will develop refractory disease
Despite compliance to GFD
Happens in 6th decade
Normal tTG IgA (or IgG)

Diarrhoea and weight loss

39
Q

Types of refractory coeliac disease

A

Type 1

  • Normal intraepithelial lymphocyte (IEL) phenotype
  • Good prognosis
  • Responds to immunosuppression - budesonide + azathioprine

Type 2

  • Abnormal intraepithelial lymphocytes with monoclonal phenotype - can predict the risk of lymphoma if loss of CD3, CD4, CD8 surface markers on flow cytometry (or immunohistochemistry). Predictive if >80% CD3e+CD8- IELs
  • 50% will develop enteropathy associated T cell lymphoma in 5 years with a 5 year survival rate of <50%
  • Variable response to rx (chemotherapy +/- ASCT)
40
Q

IgG4 disease

A

Systemic, fibroinflammatory disease
Typically affects pancreas, bile ducts, retroperitoneal fibrosis, aortitis

Previously a lot of people have had unnecessary surgery (Whipples) when there’s been lumps in the pancreas
Now must do IgG4 level to confirm its not just IgG4 disease - avoid surgery

41
Q

Diagnosis IgG4 disease

A

IgG4 level

Histology/aspirate

42
Q

Rx IgG4 disease

A

Don’t need treatment if asymptomatic

Symptomatic (immunosuppression)
1st line: steroids then wean
Recurrence: azathioprine (first line), MTX, mycophenolate
Refractory: rituximab

43
Q

ERCP indications

A

Mostly done as a therapeutic procedure

1) Obstructed bile ducts confirmed on USS, CT scan, CT cholangiogram or MRCP
2) Gallstone pancreatitis AND cholangitis

3) Primary sclerosing cholangitis if inadequate imaging
(only diagnostic indication) or biliary obstruction

4) Sphincter of Oddi dysfunction
- Type 1: typical biliary colic + abnormal pancreatic enzyme + abnormal imaging + abnormal LFTs
- Type 2: abnormal imaging + blood tests

44
Q

If bilirubin >50 in obstructed bile ducts, should avoid which investigation?

A

CT angiogram (bile ducts won’t show up)

Do MRCP

45
Q

Complications ERCP

A

5% pancreatitis (reduced by indomethacin suppository)
1% bleeding
1% perforation
1/1000 mortality

46
Q

Iron deficiency anaemia or unknown cause or overt GI blood loss
What investigations to do?

A

Pill cam –> double balloon enteroscopy to treat the lesion (invasive procedure; anterograde requires intubation; retrograde doesn’t)

If negative pill cam, won’t generally proceed to a double balloon. May need CT enterography or MR enterography first to look for funny lesions.

Gastroscopy + colonoscopy miss 5m of small bowel.

Need CTAP if suspicious of malignancy

47
Q

Why do MRCP over CT cholangiogram for obstructive bile duct?

A

Jaundice patients

  • Do US first but doesn’t show good images around duodenum i.e. CBD or ampulla
  • Plain CT may be adequate but 90% gallstones are cholesterol so wont’ be visible on CT
  • To show up bile ducts, needs CT cholangiogram. However if bilirubin >50, the contrast that is used in CT is not adequately excreted into the bile ducts if they are jaundiced or have high bilirubin.
  • MRCP can be done in jaundiced patients. But may not get good quality images due to breath holding factors, hence if bili is <50, should do CT cholangiogram
  • In young PSC patients, MRCP is better because they’re going to need lifelong scanning
48
Q

When is a red cell scan used?

A

Not used much anymore

If there is enough bleeding >1ml/min, red cell scan can work. Used when desperate.

49
Q

Is ETOH a risk factor for PUD?

A

No

50
Q

Oesophagus is made up of 2 muscle layers

What are they? What lies inbetween?

A

Inner circular
Outer longitudinal

Plexus of nerves lie inbetween the two layers and also on the submucosal side

51
Q

Oesophagus
Upper 1/3 is …
Lower 1/3 is …
Middle 1/3 is …

A

Straited
Smooth
Mixed

52
Q

Risk factors for GORD

A 
Age
Obesity (central)
Hiatus hernia
Pregnancy
Scleroderma
Asthma
Smoking
Alcohol
53
Q

Does H.pylori cause GORD?

A

NO

Protects against GORD actually!

54
Q

Is GORD genetic?

A

Yes

Relatives of patients with GORD or Barrett’s are more likely to have frequent reflux symptoms

55
Q

Mechanism of GORD

A

Transient lower oesophageal sphincter relaxation
- Some reflux is physiological (burping)

Weak lower oesophageal sphincter

Increased intraabdominal pressure (obesity)

56
Q

Complications of GORD

A 
Ulceration/bleeding
Strictures
Barrett's
Adenocarcinoma of oesophagus
Pharyngeal reflux - sore throat
57
Q

Is recumbent reflux normal?

A

No

Its always abnormal

58
Q

Are GORD symptoms predictive of oeosphagitis or severity of oesophagitis?

A

No

59
Q

When to investigate further in GORD?

A

Dysphagia, weight loss, haematemesis
Refractory to simple therapy 4/52 PPI (8/52 if severe)

No evidence to look for Barrett’s oesophagus in longstanding symptoms

60
Q

GORD symptoms

A

Heartburn
Regurgitation of gastric contents, effortness

Non-specific/extra-oesophageal

  • Nausea, epigastric pain
  • Cough, worsening asthma
  • Chest pain
  • Sleep disturbance
  • Dental problems
61
Q

Dysphagia in longstanding GORD DDx

A

Oesophagitis
Stricturing
Malignancy

62
Q

Should we do surgery i.e. fundoplication in GORD?

A

Indicated in failed medical therapy

Effective in symptom control

Disadvantages

  • Complications and 0.1% mortality
  • Everyone gets excess flatus and limited period of dyaphgia
  • Occasionally get severe dysphagia, gas bloat, inability to belch, vomit, paraoesophageal hernia
  • Can fail with time
63
Q

What investigations should we do pre-op before considering fundoplication in GORD?

A

Manometry study
- Make sure its not achalasia or oesophageal hypomotility that’s causing GORD symptoms

Endoscopy
- May show oesophagitis

pH study
- If endoscopy doesn’t show oesopahgitis. Confirms excessive acid exposure. Especially if there are atypical symptoms

64
Q

2 types of oesophageal cancer

A

SCC (incidence reducing)
- Smoking

Adenocarcinoma (majority)
- Major risk factor is Barrett’s

65
Q

How to take appropriate biopsies for Barrett’s?

A

4 quadrant biopsies at 1cm intervals is required within the Barrett segment

Also should wait after healing as inflammatory changes can interfere with assessment of dysplasia (reactive atypia)

66
Q

Investigation of oesaphgeal dysphagia

A

Endoscopy

  • Sees mucosa
  • Can biopsy e.g. eosinophilic oesophagitis
  • Can be therapeutic e.g. dalatation

Barium swallow

Oesophageal manometry
When endoscopy and barium swallow haven’t demonstrated a cause

67
Q

What’s distal oesophageal spasm?

A

Synchronous, uncoordinated contractions of SM of the oesophageal body

68
Q

Presentation of distal oesophageal spasm

A

Dysphagia

  • Often variable
  • Cold liquids, large boluses
  • May get impaction

Chest pain

Regurgitation

69
Q

Diagnosis of distal oesophageal spasm

A

Barium swallow

  • Tertiary contractions
  • Diverticulae
  • Poor passage of bolus

Endoscopy

  • Retained food
  • Uncoordinated or ring contractions

Manometry
- Synchronous pressure waves

70
Q

Management of distal oesophageal spasm

A

Soft foods
Eat slowly
Wash down with water

CCB
GTN spray
PPI

Botox into oesophageal body
Dilatation
Myotomy (POEM)

71
Q

When to transfuse for upper GI bleed?

A

Aim Hb 70-90

Aim Hb ≥90 in IHD

72
Q

How to risk stratify for upper GI bleed pre-endoscopy?

A

Blatchford score
Score <1 = low risk, OP endoscopy

Urea
Hb
SBP
HR >100
Melena 
Syncope
Hepatic disease
Cardiac failure
73
Q

How to predict risk of recurrent GI bleed and mortality post-endoscopy?

A

Forrest score
- Endoscopic appearance of ulcer

Rockall score

  • Age, haemodynamic shock, comorbidities, diagnosis, recent haemorrhage
  • Predicts rebleeding and mortality

AIM 65

  • Albumin, INR, mental state, SBP, Age
  • Predicts mortality
74
Q

How soon should we do gastroscopy for non-variceal GI bleed?

A

Within 24 hours

Data is conflicting re urgent endoscopy for high risk patients - could make things worse as patients are not adequately resuscitated and not had PPI to reduce ulcer stigmata

75
Q

Should PPI be used in upper GI bleed (non-variceal)?

A

YES
IV esomeprazole 80mg (push over 15-30 minutes) then 8mg/hr infusion

Pre-endoscopy - reduces rates of high risk stigmata and need for endoscopic therapy

But most evidence is in post endoscopy - given 72h post endoscopy for high risk ulcers is associated with reduction in re-bleeding, blood transfusion requirements, hospital LOS, mortality

76
Q

Endoscopic treatment options for bleeding PUD

What to do in recurrent bleed?

A

Dual therapy is standard treatment
Inject with adrenaline AND either clip or cauterize or inject sclerosant

Recurrent bleed
Repeat endoscopy with endoscopic hemostasis
If haemostasis not achieved or recurrent rebleeding following 2nd attempt, consider:
Over the scope clips (OTSC) aka bear claw
Topical haemostatic spray
Refer for transcatheter angiographic embolisation (TAE) or surgery

77
Q

Where do varices commonly happen?

A

Oesophageal > gastric

78
Q

What’s the risk of variceal Haemorrhage? What increases the risk of bleed?

A

5-15% per year

Increased risk of bleeding

  • Large varix (30% annual risk of bleed)
  • Child pugh C > B > A
  • Red sign, red wale mark
  • Ongoing ETOH
  • HVPG >12mmHg
  • Previous bleed (60-70% annual risk)
79
Q

What is the preferred endoscopic treatment for gastric varices?

A

Glue injection!

For oesophageal varices, banding is 1st line

80
Q

What are the disadvantages of glue injection for gastric varices management?

A

Embolisation

E.g. splenic infarct, pulmonary infarct

81
Q

DDx of melena

A 
Variceal bleed
PUD (duodenal > gastric)
Mallory-Weiss tear
Malignancy
Reflux oesophagitis
Gastric erosion/gastritis
82
Q

Severe Haematochezia - what are you worried about?

A

10-15% have an upper GI bleed!

If the suspicion is high, must do gastroscopy to exclude
If the suspicion is moderate, can do nasogastric lavage (coffee ground material or bright red blood in the lavage fluid)

83
Q

Consequences of undiagnosed coeliac disease

A

Increased all cause mortality

Impaired QOL - impaired fertility, osteoporosis

84
Q

What part of gluten is immunogenic?

A

Gliadin

85
Q

When to screen for coeliac disease with serology

A 
Persistent unexplained GI symptoms
Faltering growth
1st degree relative with coeliac
Autoimmune thyroid disease
IBS (in adults)
Prolonged fatigue
Unexpected weight loss
Severe or persistent mouth ulcers
Unexplained iron, B12, folate deficiency
T1DM

Consider
Metabolic bone disorder
Unexplained neurological symptoms (peripheral neuropathy, ataxia)
Unexplained subfertility or recurrent mismarriage
Persistent elevated liver enzymes with unknown cause
Dental enamel defects
Down’s syndrome
Turner’s syndrome

86
Q

How to monitor coeliac response after starting GFD?

A
  • Repeat ab level after 6/12 gluten free diet
  • Antibodies generally return to normal after 12/12
  • Mucosal healing takes 18 months-2 years
  • Repeat gastroscopy and biopsy is useful in adults to assess/confirm of goal of mucosal remission
87
Q

Should we screen family members of patients with coeliac disease?

A

YES

10% risk of also having coeliac disease

88
Q

Is gluten free diet beneficial for non-coeliac people?

A

NO

Linked to CV events!! (due to reduction in cardioprotective whoe grain intake)

89
Q

Is coeliac serology a reliable indicator of disease activity?

A

No

Gastro (9 decks)

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