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G.I. > Dyspepsia and PUD > Flashcards

Dyspepsia and PUD Flashcards

1
Q

Dyspepsia

A

epigastric pain/burning

post-prandial fullness

early satiety

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2
Q

Causes of dyspepsia

A

> Peptic ulcer disease
H pylori
NSAIDs
Gastric cancer

Idiopathic (majority) - FUNCTIONAL
No evidence of culprit structural disease

GORD may coexist

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3
Q

Dyspepsia - o/e

A

Uncomplicated - epigastric tenderness

complicated - cachexia, mass, evidence of gastric outflow obstruction, peritonism

gastric outflow obs - succussion (sloshing)

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4
Q

If no ALARM symptoms - treatment?

A

Check H pylori
Eradicate if infected
If HP -ve, treat with acid inhibition.

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5
Q

What is HEARTBURN/reflux?

A

Gastro Oesophageal Reflux Disease

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6
Q

Functional dyspepsia?

A

Presence of one of:

epigastric pain/burning

post-prandial fullness

early satiety

No evidence of structural disease.

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7
Q

Peptic Ulcer Disease

A

> Pain is predominant dyspepsia
Cause of dyspepsia
Aggravated or relieved by eating
Relapsing and remitting chronic illness

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8
Q

Causes of peptic ulcer disease

A

H pylori

NSAIDs

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9
Q

Helicobacter pylori

A

> Acquired in infancy
Gram negative microaerophilic flagellated bacillus

> Oral-oral, faecal-oral spray

> Consequences do not arise until later in life

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10
Q

Consequences of H pylori infection

A
  1. Nothing
  2. Peptic Ulcer Diseaese
  3. Gastric cancer (rare)
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11
Q

What does H pylori do?

A

Causes an increase in acid secretion and gastrin release (leading to more acid secretion)

Duodenal acid load increases –> gastric metaplasia in the duodenum

H pylori can then colonise these “islands” of metaplasia leading to ULCERATION

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12
Q

If edges of ulcer are irregular, what could that entail?

A

Possible cancer

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13
Q

Gastric atrophy - appearance of mucosa

A

No rugae

Flat AF

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14
Q

Acute gastritis - appearance

A

Folds are puffed up and flattened out

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15
Q

H pylori - diagnosis

A

Gastric biopsy
Urease test
Histology
Culture/sensitivity

Urease breath test

Faecal antigen test

IgA antibodies

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16
Q

What does H pylori use as one of its energy sources?

A

Urea

Hence urease breath test is used to detect presence of h pylori

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17
Q

Treatment of peptic ulcer disease

A

ALL antisecretory therapy (PPI, Histamine receptor antagonists): 4-8 wks therapy

OMEPRAZOLE in particular

Test for presence of H pylori//

If positive - eradicate and confirm

If negative - antisecretory therapy

Withdraw NSAIDs

Nutrition for non HP/NSAID ulcers.

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18
Q

H pylori eradication therapy

A

Triple therapy for 1 week
- PPI + amoxycillin (1g bd) + clarithromycin 500mg bd

  • PPI + metronidazole 400mg bd + clarithromycin 250mg bd

2 week regimens//

higher eradication rates
poorer compliance

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19
Q

Peptic ulcer disease - complications

-

A

anaemia
bleeding
perforation
gastric outlet obstruction

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20
Q

Gastric ulcer follow up

A

Endoscopy at 6/8 wks

Ensure healing and no malignancy

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21
Q

IL-1B (interleukin 1B) inflammatory host H pylori causes?

A

Gastric cancer

Acid HYPOsecretion (not the usual high acid)

Body predominate gastritis

Atrophic gastritis

Cancer

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22
Q

What does the oesophagus NOT possess?

A

A serosa

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23
Q

Main cancers of the oesophagus?

A

Adenocarcinoma (mainly)

Squamous cell carcinoma

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24
Q

Barrett’s Oesophagus

  • related to
A

Chronic GORD related

replacement of stratified squamous epithelium by columnar epithelium

Metaplasia

THEN becomes dysplastic –> Adenocarcinoma

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25
Q

New onset dysphagia in an over 55 = [investigation]

A

Endoscopy

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26
Q

Mucosal abnormality = x biopsies

A

6

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27
Q

Staging of oesophageal cancer

A

PET CT - more sensitive for distal node disease

Endoscopic ultrasound - regional nodal disease

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28
Q

TNM staging for oesophageal cancer

A 
T = how far primary tumour has grown into wall 
N = Cancer spread to nearby lymph nodes
M = Metastasis

Tis = tumour in situ
T1a = endoscopic management of cancer
T1b -> T4b - must be removed by oesophagectomy

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29
Q

Where are squamous cell carcinomas more commonly found in oesophagus

A

More proximally

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30
Q

Squamous cell carcinoma treatment

A

Localised SCC - radical chemoradiotherapy

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31
Q

Adenocarcinoma

A

May be suitable for endoscopic resection (if Tis or T1b)

No metastases –> consider oesophagectomy ± chemo

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32
Q

Upper GI haemorrhage - the “100” rule

A 
Poor prognostic group
Systolic BP < 100mmHg
Pulse > 100
Hb < 100g/l
Age> 60
Comorbid disease
Postural drop in blood pressure
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33
Q

Upper GI bleed - endscopy

A

Identify cause
Therapeutic manoeuvres
Assess risk of rebreeding

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34
Q

Blatchford Score

A

0-1 = low risk GI bleed
2-5 = indeterminate risk
≥ 6 = HIGH RISK GI BLEED

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35
Q

Treatment of GI bleed

A

If witnessed significant bleeding or stigmata - IV omeprazole infusion

If stigmata of cirrhosis/ known liver disease = TERLIPRESSIN

For high risk –> endoscopy ASAP

36
Q

What drug is used for an intermediate/high risk GI bleed??

A

TERLIPRESSIN (if stigmata of liver cirrhosis/disease)vis

37
Q

Endoscopic treatment of peptic ulcers

A
  1. Injection
  2. Heater probe coagulation
  3. Combinations
  4. Clips
  5. Haemospray
38
Q

Peptic ulcer endoscopic treatment

A

1st line - adrenaline injection/ heater probe

If re-bleed, use omeprazole infusion

Further therapy.

Bleed stops.

Then omeprazole
H pylori eradication as appropriate

If bleeding continues –> SURGERY

39
Q

Variceal bleeding - risk factors

A

Portal hypertension > 12mmHg

Cirrhotics with varies will bleed < 2 years

Degree of liver failure

High mortality

40
Q

Variceal bleeding - haemostasis

A
  1. Terlipressin
  2. Endoscopic variceal ligation (banding)
  3. Sclerotherapy
  4. Sengstaken-Blakemmore balloon
  5. TIPS
41
Q

Where are varices most common?

A

Bottom 5cm of the oesophagus

42
Q

Terlipressin

A

Vasopressin prodrug

Splanchnic vasoconstrictor

Beneficial for renal perfusion

43
Q

If endoscopic homeostasis fails, what then?

A

Sengstaken-Blakemore Tube

balloon; inflate balloon and pul back - puts pressure on GO junction

44
Q

TIPSS (Transjugular intrahepatic portosystemic shunt)

A

Uncontrollable bleeding gastric varices

FINAL LINE

45
Q

Acute oesophagitis

A

Rare

CORROSIVE damage following chemical ingestion

46
Q

Chronic Oesophagitis

A

Common

REFLUX disease

(rare causes include Crohn’s)

47
Q

Reflux oesophagitis

  • due to
  • raised intra-abdo pressure in…
A

Inflammation of the oesophagus due to reflux of gastric content (acidic)

Defective sphincter ± hiatus hernia

Raised intra-abdominal pressure due to obesity or pregnancy

48
Q

What are the cells most associated with chronic inflammation?

A

Macrophages and lymphocytes

49
Q

Reflux oesophagitis - histology

A

Basal zone expansion

Increased proliferation to compensate for increased cell desquamation

Elongation of papillae

50
Q

Complications of reflux

A

> Ulceration
Stricture
BARRETT’S OESOPHAGUS (untreated)

51
Q

Barrett’s oesophagus (looks like a material)

A

Red velvety oesophagus

52
Q

What is metaplasia at risk of developing into?

A

Dysplasia and cancerous growth

53
Q

Is Barrett’s oesophagus a pre malignant condition?

A

Yes

54
Q

Allergic Oesophagitis

  • ## what kind of cells?
A

Eosinophilic oesophagitis

Asthma/allergy

Corrugated (feline) oesophagus

Looks like a trachea

55
Q

Allergic oesophagitis - treatment

A

Steroids, chromoglycate, montelukast

56
Q

Benign Oesophageal Tumours

A

> Squamous papilloma

- Related to HPV 
- Rare

> Leiomyomas
Lipomas
Fibrovascular polyps
Granular cell tumours

57
Q

Malignant oesophageal tumours

A

> Squamous cell carcinoma - “islands of malignant cells”

> Adenocarcinoma

DYSPHAGIA

58
Q

Squamous cell carcinoma is more common amongst?

A

Iranians, Chinese

Very hot tea

59
Q

HIGH grade dysplasia

A

Cells look malignant but have not yet intended basement membrane

60
Q

Mechanisms of metastases

A

> Direct invasion
Lymphatic permeation
Vascular invasion

61
Q

General symptoms of malignancy

A

> Anaemia
Weight loss, loss of energy
Due to effects of metastases

62
Q

Boerhaave syndrome

A

Spontaneous perforation of the oesophagus due to retching or vomiting (also barretts)

Most commonly occurs in distal oesophagus

Left

Severe retrosternal chest pain

Odynophagia

Mediastinal/ free peritoneal air

63
Q

Oral Squamous Cell carcinoma

A

White, red, speckled, ulcer, lump.

Floor of mouth, lateral border and ventral tongue

Soft palate

64
Q

Chemical gastritis

A

Due to NSAIDs, alcohol, bile reflex

Direct injury to mucous layer

Hyperplasia and little inflammation

Erosions/Ulcers form

65
Q

Chronic duodenal ulcers

A

50% of patients with duodenal ulceration have increased acid secretion

Excess acid in duodenum –> metaplasia –> H pylori infection –> inflammation –> ulceration

66
Q

Peptic ulcer - microscopic

A

Layered

Floor of necrotic pus
Inflammation
Fibrotic scar tissue (deepest)

67
Q

Complications of peptic ulcers

A 
Peforation
Penetration
Haemorrhage
Stenosis
Intractable pain
68
Q

Autoimmune gastritis

A

Rare

Anti-parietal and anti intrinsic factor antibodies

Atrophy/intestinal metaplasia

Pernicious anaemia due to B12 deficiency

Malignancy risk

69
Q

Gastric Adenocarcinoma - premalignant conditions

A

H pylori is a big cause

Pernicious anaemia

Partial gastrectomy

lynch syndrome
menetrier;s disease

70
Q

Gastric adenocarcoma - subtypes

A 
> Intestinal type//
 exophytic/polypoid mass
cauliflower like
raised edges
heaped up border
not very well defined borders

> Diffuse type//

expands/infiltrates stomach wall

signet ring sign
can spread
they do not aggregate

WORSE PROGNOSIS

71
Q

Maltoma (MALT)

A

Derived from mucosa associated lymphoid tissue

H pylori infection

Continuous inflammation induces an evolution into a clonal B cell proliferation

If unchecked becomes a high grade lymphoma

“creamy”
“Fleshy”

72
Q

Benign gastric tumours

A

Polyps
Hyperplastic polyps
Cystic fund gland polyps

73
Q

Linitis plastica

A

Diffuse type

“Leather bottle stomach”

Malignant

74
Q

GORD

3 factors

A

> Incompetent LOS
Poor oesophageal clearance
Barrier function/visceral sensitivity

75
Q

Symptoms of GORD

A 
Heartburn
Acid reflux
Waterbrash
Dysphagia
Odynophagia
Weight loss
Chest pain
Hoarseness
Coughing
76
Q

GORD - Ix

A

Endoscopy

Oesophageal manometry & pH studies

77
Q

Management of GORD

A

Symptom relief//

Stop smoking
lose weight
prop up the bed head

antacids - PPIs***, H2RAs

Healing oesophagitis//

surgery (nissen fundoplication)

Prevent complications//

78
Q

Nissen Fundoplication (GORD)

A

Controls symptoms of GORD well

Heals oesophagitis

Young patients

Severe/ unrespons disease

Wrapping fundus around oesophagus - reinforcing the closing function of the LOS

79
Q

Dysplasia management

A

Surveillance every 3 months
Endoscopy

Optimise PPI dose

80
Q

Gastroparesis

A

Delayed emptying of stomach

No physical obstruction

Fullness
Nausea
Vomiting
Weight loss
Upper GI pain
81
Q

Causes of gastroparesis

A

Idiopathic
Diabetes mellitus
Cannabis
Medication - opiates, anti ACh

82
Q

Gastroparesis - management

A

Removal of drugs

Liquid diet

Eat little and often

Promotility agents

83
Q

Achalasia

What is it?
What happens to the food?

A

Failure of sphincter smooth muscle to relax

Food backed up in oesophagus

Heller myotomy

84
Q

Heller myotome

A

Muscles of cardia are cut, allowing food and liquids to pass into stomach .

85
Q

Consequences of vomiting

A 
Dehydration
Hypochloraemic 
Metabolic alkalosis
Hypokalaemia 
Mallory weiss tear
Aspiration of vomitus

G.I. (20 decks)

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