3.2 Peptic Ulceration

Digestion

serves to convert food stuffs into manageable units to get across SI

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Abnormalities of Digestion and Absorption

Some genetic disturbances as a consequence of the absence of specific enzymes, e.g. lactose intolerance

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1st step of digestion - mastication

chewing, grind up and break up food for swallowing, mix food with saliva, stimulate taste buds

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Saliva

contains electrolytes produced by 3 main pairs of branched glands (original secretion changed before getting to mouth), parotid(cheek), sublingual (under chin), submandibular (under tongue), derived from plasma

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Functions of Stomach

storage of food, initiation of digestion of proteins, kill ingested bacteria (via acid), formation of chyme, before transfer to SI

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Storage

can accommodate large vol, initially relaxes when 1st start eating, pressure doesn't increase much due to distention of stomach wall and reflex (vagal) inhibition of SM tone, rate of release regulated

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Adventitia

the outer wall of gut tube, thin layer of gut tube

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Serosa

covered in serous membrane

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Serous membrane

squamous epithelial cells secreting a small amount of fluid to allow organs to glide over each other

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Gut Associated Lymphoid Tissue (GALT)

lymphoid tissue located in lamina propria, ranges from individual (T cells, macrophages) to large aggregates composed of T and B lymphocytes

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Payer 's patches

feature of ileum of SI, overlain by antigen sampling cuboidal cells

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Mucosa

epithelium, basement membrane, lamina propria (connective tissue, blood vessels, nerves), muscular mucosa (thin layer of SM)

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Submucosa

connective tissue, blood, lymph and nerves, aggregates of lymphoid tissue, GALT, hands may lay here

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Muscularis

SM layers

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Adventitia/Serosa

connective tissue, blood, lymph and nerves, serosa is associated with peritoneum

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Nerve supply

submucosal and myenteric plexiglass control contraction of muscles in waves to move food along tract, modulated by autonomic nervous system (parasympathetic NS is stimulatory)

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Stomach secretion

~2L of gastric juice per day, arises from cells lining the stomach, gastric mucosa

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gastric mucosa

Oxyntic mucosa (in funds and body), pyloric gland area (in antrum), mucoasal gland cells found in gastric pits (bottom of fold), mucosal neck cells at top, impermeable so anything produced won't move back up

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Gastric Phase

when food reaches stomach, gastric secretion increased, occurs due to local sago-vagal reflexes in response to mechanical stimulation, due to food in antrum, stimulation of gastrin release from G-cells by peptide fragments of part digested proteins

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Intestinal Phase

~5% gastric secretions, due to circulating aa or gastrin, when food goes into SI, negative feedback loop stopping HCl release

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Comensal Flora

resident, normally harmless, beneficial

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Transient Flora

microorganisms that reside for a short time in a particular site, without damage of the host

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Opportunists

capable of invading or damaging normal host, capable of invading or damaging when immunity compromised

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Colonisation

all normal flora sites are colonised, with characteristic pop, begins at birth through vaginal coal, flora can change during puberty/menstration, tissue surfaces have specific receptors

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Infection by normal flora

if normal fora gains access to sites normally sterile, infection may result, assisting factor usually needed such as surgery, immune suppression or failure of normal physical barriers

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Summary of Factors Leading to Opportunistic Infection

compromised immunity, can be due to effects of antibiotics on normal flora, breach of physical barriers, impaired normal clearance mechanisms

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Physical and Chemical Barriers Host Defences

stomach acid, digestive enzymes, mucosal lining and mucin, continuous movement

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Immune System Host Defences

Secreted IgA and Payer's Patches

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Bacterial Culture

can use selective agar that has antibiotics and other things that kill the other bacteria so others can go, can have UV colour changes which is specific bacteria

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Antigen/Toxin Testing

for detecting specific target, used routinely in lab to test for viruses, Ines appear if have antigen

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Microscopy

only useful for parasites which are larger and easier to see, sample concentrated to improve sensitivity

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Viral gastroenteritis

face-oral spread, explosive diarrhoea often with vomiting, incubation 24-48hr, detect by antigen teasing or PCR

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E. coli

common, short incubation (~12hr), lab diagnosis not possible, oral hydration

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E.Coli 0157

can cause hemolysis and renal failure, mediated by toxin production, attach to dining of gut and pump toxins into blood stream, and destroy rbc, antibiotics could aggravate HUS

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Campylobacter

main source is raw chicken, presents with diarrhoea, abdominal cramps, sometimes vomiting, incubation 2-5 days, culture with selective agar, usually self-limiting

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Shigella

several species, can cause bloody diarrhoea, low infectious dose, cultured with selective agar, supportive treatment

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Toxin mediated food poisoning

incubation - hours, enterotoxin induced, can be heat stable toxins, self-limiting

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Parasites

water-borne from faecally contaminated water supplies, often travel related, incubation: 7-10 days, some can causes diarrhoea

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Biequivalence

identical rate & extent of absorption, assessed by: tmax, peak plasma level (Cmax), bioavailability (F)

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Morphine

opoid analgesic, T1/2~2-3 years, oramorph (oral suspension for immediate pain relief), morphogenic SR (sustained 12hr release)

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Nifedipine

DHP Ca channel inhibitor, hypertension and angina, t1/2~2hr, immediate release prep associated w increased cardiac event

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Polymers for enteric coating

Take whole as unstable in acid, broken down down in less acidic environment in duodenum

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Alginates

originally derived from seaweed, my be combined, alginic acid when combines with saliva forms viscous foam, floats on gastric contents forming raft which protects oesophagous during reflex

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Ulcerogenic Effects of NSAIDs (and Oral Steroids)

oral NSAIDs (commonly) and corticosteroids (less commonly) associated with peptic damage/ulceration NSAIDs - aspirin, ibuprofen, diclofenac, naproxen

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Cyclooxygenases

exists in 2 isoforms- COX-1 (physiological, gastric protection), COX-2 (pathological, inflammation), most NSAIDs inhibit both (damage), COX-2 more specific so less side effects

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Health inequaities

differences in health status or in distribution of health determinants between different population groups

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Health inequities

avoidable inequalities in health between groups of people within countries and between countries

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Index of Multiple Deprivation (IMD)

• Official measure of relative deprivation for small areas, • Combines information on income, employment, education, crime, housing and living environment

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3.2 Peptic Ulceration

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