Upper GI Disease Flashcards

1
Q

Dyspepsia Definition

A

group of symptoms

• PAIN/DISCOMFORT IN UPPER ABDOMEN

• RETROSTERNAL PAIN, HEARTBURN
• ANOREXIA, NAUSEA, VOMITING BLOATING, FULLNESS/EARLY SATIETY
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2
Q

Dyspepsia Investigations

A

Hx + examination

* Drug hx = NSAIDs, steroids, bisphosphonates, CCB, nitrates, theophyllines, anti-muscarinics, OTT drugs to help symptoms
* Lifestyle/PMHx hx = diet (fat, alcohol, large meals, coffee), systemic sclerosis, achalasia rx, hiatus hernia, pregnancy/obesity, smoking, exercise

Bloods = FBC, ferritin, LFTs, U+Es, calcium, glucose, coeliac serology, serum IgA

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3
Q

ALARMS Symptoms

A

ANOREXIA (UNEXPLAINED)

LOSS OF WGT. (UNEXPLAINED)

ANAEMIA: IRON DEFICIENCY - COULD SIGNIFY LESION IN GI THAT IS BLEEDING

RECENT ONSET&raquo_space; 55YRS/PERSISTENT DESPITE TREATMENT

MELAENA/HAEMATEMESIS/MASS

SWALLOWING PROBLEMS - DYSPHAGIA (esp. if constant & increasing in freq.)

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4
Q

Dyspepsia Aetiology

A

Organic/Functional

H. PYLORI

Upper GI = peptic ulcer, gastritis, non-ulcer dyspepsia, gastric cancer

Hepatic Causes, Pancreatic Disease, Gallstones

Lower GI = coeliac disease, IBS, colonic cancer

Psychological
Drugs
Other system disease = metabolic, cardiac, hypercalcaemia, DM

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5
Q

H. pylori - bacterial characteristics, outcomes + what do outcomes depend on

A

gram -ve bacteria + microaerophilic + spiral shaped + flagellated - faecal-oral route

can only colonise gastric-type mucosa + reside in surface mucus layer - uses flagella to burrow into mucus layer to survive aci & produces urease to produce alkaline layer ~ it

evokes immune response in underlying mucosa - depends on host factors

Outcome depends on = site of colonisation, bacterial characteristics, host factors, environmental factors

Can result in = ASYMPTOMATIC/CHRONIC GASTRITIS (most likely), CHRONIC ATROPHIC GASTRIC & INTESTINAL METAPLASIA, GASTRIC/DUDENAL ULCER, GASTRIC CANCER; MALT LYMPHOMA (v. unlikely)

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6
Q

H. pylori - diagnosis

A

Non-invasive = serology (IgG against H. pylori - unspecific), 13C/14C UREA BREATH TEST (looks for urease presence by measuring CO2), STOOL ANTIGEN TEST (ELISA, off PPI for 2 weeks)

Invasive = gastric biopsies (for histology + culture), RAPID SLIDE UREASE TEST (CLO) - looks for urease presence by looking for ammonia

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7
Q

Gastritis

A

Aetiology:

A = autoimmine, rare, autoantibodies attack parietal cells - lose specialised epithelium = reduced acid secretion + pernicious anaemia

B = BACTERIAL, H. PYLORI

C = CHEMICAL, BILE, DRUGS e.g. NSAIDs, alcohol

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8
Q

Peptic Ulcer Disease Risk Factors

A
H. pylori
Smoking
Alcohol
Drugs e.g. NSAIDs
Stress

Rare = crohn’s disease, Zollinger-Ellison syndrome, hyperparathyroidism

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9
Q

Peptic Ulcer Disease Epidemiology

A

COMMON, decreased incidence in developing countries

MEN > WOMEN & DU > GU (but both common in elderly)

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10
Q

Peptic Ulcer Disease Presentation

A
  • EPIGASTRIC PAIN = MAIN FEATURE; MAY BE RELIEVED BY ANTACIDS
    • NOCTURNAL/HUNGER PAIN (MORE COMMON IN DU = may be due to malabsorption due to ulcer)
    • BACK PAIN (MAY SUGGEST PENETRATION OF POSTERIOR DU; as DU would be low down & back pain will be evident if ulcer perforates & damages posterior structures)
    • NAUSEA, VOMITING (occasionally; IF BLEEDING ULCER = HAEMATEMESIS &/OR MELAENA, ANAEMIA), ANOREXIA, WGT. LOSS
    • EPIGASTRIC TENDERNESS MAY BE ONLY SIGN
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11
Q

Peptic Ulcer Disease Management

A

• MEDICAL:

	○ ERADICATION THERAPY IF ULCERS CAUSED BY H. PYLORI

	○ ANTACIDS - PPI (omeprazole)/H2 ANTAGONISTS (ranitidine)

	○ IF NSAIDS INVOLVED = STOPPED/IF CONTINUED MUST RECEIVE PROTECTIVE AGENTS FOLLOWING ERADICATION THERAPY

	○ TREAT COMPLICATION AS THEY ARISE

• SURGERY: ONLY FOR COMPLICATED PUD
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