The Death of an Operation

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Symptoms and Signs

Symptoms depend on ulcer location and patient age; many patients, particularly the elderly, have few or even no symptoms. Pain is the most common symptom; it is often localized to the

epigastrium and relieved by food or antacids. The pain is described as burning, gnawing, or hunger. The course is usually chronic and recurrent. Only about half of patients present with the

characteristic pattern of symptoms.

PEPTIC ULCER DISEASE

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Vagus (CN X)

From 1940’s – 1990’s highly selective vagotomywas the primary treatment for peptic ulcer disease

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H. pylori

normal gastric mucosa

H. pylori colonization

normal gastric mucosa

colonized gastric mucosa

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H. pylori is gram-negative spiral flagellated bacterium Produces urease

Important in the etiology of peptic ulcers and gastric cancer Found in:

90% patients with duodenal ulceration 70% patients with gastric ulceration

60% patients with gastric cancer

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The organism can be detected by: Microscopy – silver or Giemsa staining of stomach biopsies Culture – difficult and requires special culture techniques Rapid urease test – colour changes due to change in pH

13C or 14C breath test – Ingested radioactive urea is broken down to carbon dioxide

Serology – detected immunologically using an ELISA

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H2 Antagonists65% healing at one month 85% healing at two months

If stop treatment - 90% recurrence at 2 years If maintenance therapy - 20% recurrence at 5 years

Proton Pump inhibitors90 - 100% healing at 2 months

Low recurrence on long term maintenance

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normal CXRsabnormal CXR

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H. Pylori eradication

80% cured with dual or triple therapy Two weeks amoxycillin, metronidazole and omeprazole

Short term recurrence rates low Long term recurrence rates are at present unknown

Drugs have changed the need for ulcer surgery over last 20 years Admissions for elective surgery have significantly reduced The number of complications however remain unchanged May be increasing due to increased NSAID use in elderly

Bleeding and perforation still have mortality of >10%

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Sensors: pressure sensors in the arteries of the upper body: Respond to stretch caused by blood pressure

Higher pressure produces more nerve impulses/sec; lower blood pressure causes fewer nerve impulses/sec Carotid sinus: sensory nerve = cranial nerve IX (glossopharyngeal)

Aortic arch: sensory nerve = cranial nerve X (vagus) Integrating Center: medulla oblongata of the brain

Sensory nerves go to nucleus tractus solitarius Detected blood pressure is compared with desired pressure (set point)

Centers used to correct blood pressure: Cardiac accelerator center: increases cardiac output: uses cardiac accelerator nerve

Cardiac inhibitor center: decreases cardiac output: uses vagus nerve Vasoconstrictor center: constricts arterioles and veins: uses spinal nerves

Constriction of blood vessels raises resistance to flow (R) Effectors:

Heart: SA Node: controls heart rate (HR)

Vagus nerve slows heart Cardiac accelerator speeds up heart

Heart muscle: controls stroke volume (SV) Cardiac accelerator nerve increases SV

No vagus fibers go to heart muscle Arteries & veins

Results: If pressure is low:

Reflex will increase cardiac output (CO = HR X SV) Reflex will constrict arterioles & veins

If pressure is high: Reflex will decrease CO

Decreased reflex activity will dilate arterioles and veins Reflex will restore correct blood pressure

P = CO X R

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