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Dyspepsia and PUD Flashcards

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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
New onset dysphagia in an over 55 = [investigation]
Endoscopy
26
Mucosal abnormality = x biopsies
6
27
Staging of oesophageal cancer
PET CT - more sensitive for distal node disease Endoscopic ultrasound - regional nodal disease
28
TNM staging for oesophageal cancer
``` 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
29
Where are squamous cell carcinomas more commonly found in oesophagus
More proximally
30
Squamous cell carcinoma treatment
Localised SCC - radical chemoradiotherapy
31
Adenocarcinoma
May be suitable for endoscopic resection (if Tis or T1b) No metastases --> consider oesophagectomy ± chemo
32
Upper GI haemorrhage - the "100" rule
``` Poor prognostic group Systolic BP < 100mmHg Pulse > 100 Hb < 100g/l Age> 60 Comorbid disease Postural drop in blood pressure ```
33
Upper GI bleed - endscopy
Identify cause Therapeutic manoeuvres Assess risk of rebreeding
34
Blatchford Score
0-1 = low risk GI bleed 2-5 = indeterminate risk ≥ 6 = HIGH RISK GI BLEED
35
Treatment of GI bleed
If witnessed significant bleeding or stigmata - IV omeprazole infusion If stigmata of cirrhosis/ known liver disease = TERLIPRESSIN For high risk --> endoscopy ASAP
36
What drug is used for an intermediate/high risk GI bleed??
TERLIPRESSIN (if stigmata of liver cirrhosis/disease)vis
37
Endoscopic treatment of peptic ulcers
1. Injection 2. Heater probe coagulation 3. Combinations 4. Clips 5. Haemospray
38
Peptic ulcer endoscopic treatment
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
Variceal bleeding - risk factors
Portal hypertension > 12mmHg Cirrhotics with varies will bleed < 2 years Degree of liver failure High mortality
40
Variceal bleeding - haemostasis
1. Terlipressin 2. Endoscopic variceal ligation (banding) 3. Sclerotherapy 4. Sengstaken-Blakemmore balloon 5. TIPS
41
Where are varices most common?
Bottom 5cm of the oesophagus
42
Terlipressin
Vasopressin prodrug Splanchnic vasoconstrictor Beneficial for renal perfusion
43
If endoscopic homeostasis fails, what then?
Sengstaken-Blakemore Tube | balloon; inflate balloon and pul back - puts pressure on GO junction
44
TIPSS (Transjugular intrahepatic portosystemic shunt)
Uncontrollable bleeding gastric varices FINAL LINE
45
Acute oesophagitis
Rare | CORROSIVE damage following chemical ingestion
46
Chronic Oesophagitis
Common REFLUX disease (rare causes include Crohn's)
47
Reflux oesophagitis - due to - raised intra-abdo pressure in...
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
What are the cells most associated with chronic inflammation?
Macrophages and lymphocytes
49
Reflux oesophagitis - histology
Basal zone expansion Increased proliferation to compensate for increased cell desquamation Elongation of papillae
50
Complications of reflux
> Ulceration > Stricture > BARRETT'S OESOPHAGUS (untreated)
51
Barrett's oesophagus (looks like a material)
Red velvety oesophagus
52
What is metaplasia at risk of developing into?
Dysplasia and cancerous growth
53
Is Barrett's oesophagus a pre malignant condition?
Yes
54
Allergic Oesophagitis - what kind of cells? -
Eosinophilic oesophagitis Asthma/allergy Corrugated (feline) oesophagus Looks like a trachea
55
Allergic oesophagitis - treatment
Steroids, chromoglycate, montelukast
56
Benign Oesophageal Tumours
> Squamous papilloma - Related to HPV - Rare > Leiomyomas > Lipomas > Fibrovascular polyps > Granular cell tumours
57
Malignant oesophageal tumours
> Squamous cell carcinoma - "islands of malignant cells" > Adenocarcinoma DYSPHAGIA
58
Squamous cell carcinoma is more common amongst?
Iranians, Chinese Very hot tea
59
HIGH grade dysplasia
Cells look malignant but have not yet intended basement membrane
60
Mechanisms of metastases
> Direct invasion > Lymphatic permeation > Vascular invasion
61
General symptoms of malignancy
> Anaemia > Weight loss, loss of energy > Due to effects of metastases
62
Boerhaave syndrome
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
Oral Squamous Cell carcinoma
White, red, speckled, ulcer, lump. Floor of mouth, lateral border and ventral tongue Soft palate
64
Chemical gastritis
Due to NSAIDs, alcohol, bile reflex Direct injury to mucous layer Hyperplasia and little inflammation Erosions/Ulcers form
65
Chronic duodenal ulcers
50% of patients with duodenal ulceration have increased acid secretion Excess acid in duodenum --> metaplasia --> H pylori infection --> inflammation --> ulceration
66
Peptic ulcer - microscopic
Layered Floor of necrotic pus Inflammation Fibrotic scar tissue (deepest)
67
Complications of peptic ulcers
``` Peforation Penetration Haemorrhage Stenosis Intractable pain ```
68
Autoimmune gastritis
Rare Anti-parietal and anti intrinsic factor antibodies Atrophy/intestinal metaplasia Pernicious anaemia due to B12 deficiency Malignancy risk
69
Gastric Adenocarcinoma - premalignant conditions
H pylori is a big cause Pernicious anaemia Partial gastrectomy lynch syndrome menetrier;s disease
70
Gastric adenocarcoma - subtypes
``` > 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
Maltoma (MALT)
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
Benign gastric tumours
Polyps Hyperplastic polyps Cystic fund gland polyps
73
Linitis plastica
Diffuse type "Leather bottle stomach" Malignant
74
GORD 3 factors
> Incompetent LOS > Poor oesophageal clearance > Barrier function/visceral sensitivity
75
Symptoms of GORD
``` Heartburn Acid reflux Waterbrash Dysphagia Odynophagia Weight loss Chest pain Hoarseness Coughing ```
76
GORD - Ix
Endoscopy | Oesophageal manometry & pH studies
77
Management of GORD
Symptom relief// Stop smoking lose weight prop up the bed head antacids - PPIs***, H2RAs Healing oesophagitis// surgery (nissen fundoplication) Prevent complications//
78
Nissen Fundoplication (GORD)
Controls symptoms of GORD well Heals oesophagitis Young patients Severe/ unrespons disease Wrapping fundus around oesophagus - reinforcing the closing function of the LOS
79
Dysplasia management
Surveillance every 3 months Endoscopy Optimise PPI dose
80
Gastroparesis
Delayed emptying of stomach No physical obstruction ``` Fullness Nausea Vomiting Weight loss Upper GI pain ```
81
Causes of gastroparesis
Idiopathic Diabetes mellitus Cannabis Medication - opiates, anti ACh
82
Gastroparesis - management
Removal of drugs Liquid diet Eat little and often Promotility agents
83
Achalasia What is it? What happens to the food?
Failure of sphincter smooth muscle to relax Food backed up in oesophagus Heller myotomy
84
Heller myotome
Muscles of cardia are cut, allowing food and liquids to pass into stomach .
85
Consequences of vomiting
``` Dehydration Hypochloraemic Metabolic alkalosis Hypokalaemia Mallory weiss tear Aspiration of vomitus ```

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