GI Physiology

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    GI Physiology

    Regulation Neural

    Hormonal

    Neural Regulation Involuntary except

    oesophagus & rectum

    Rest AutonomicENS

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    Extrinsic Innervation

    Somatic / Autonomic

    Somatic Pharynx & prox. Oe. (Motorlower cranial nerves

    Anal canal pudendal nerve

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    Autonomic NS

    PSNS Vagus Increases GI motility (A

    SNS Inhibit GI activity (Norad)

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    Intrinsic Innervation

    By ENS

    Afferents from gut

    Response with or without ANS

    little brain of gut

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    Hormonal Regulation

    1. Gastrin (Antrum) Increase of LESpressure, stim of small bowel and GB

    2. CCK (Duo & Jej) - Stim of GB, slowsmotility of small bowel & stomach

    3. Secretin (Duo & Jej) Increases pyloricpressure, inhibits small & large bowel

    4. Motilin (Duo) increase of gastricemptying

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    Hormonal Regulation

    5. Somatostatin (Islets) Increasesgastric emptying, inhibits secretions

    6. GIP (small intestine) Delays gastricemptying

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    Oesophagus

    Sphincters prevent regurg. and keep oe.empty between swallows

    UES prevents regurg to pharynx

    LES - prevents regurg

    maintains HPZ

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    Stomach Functions

    1. Reservoir : 200 1500ml

    2. Mix and grind food

    3. Chemically breakdown food 4. Kill microbes

    5. Control emptying into duodenum

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    Stomach Glands

    Mucous cells mucous for protection

    Parietal cells HCl & IF

    Chief cells - Pepsinogen

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    Stomach Innervation

    Vagus Increased motility & secretions

    Relax fundus on food intake

    Sympathetics Decreased activity ofsmooth muscle

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    Small Bowel

    Mucosal surface increased by plicae, villiand microvilli (500 fold)

    Motility influenzed by ANS,ENS andhormones

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    Functions of Colon

    1. Absorption of water and electrolytes

    2. Transportation of waste

    3. Storage of waste

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    Anal Canal

    Internal sphincter Involuntary,Responsible for resting pressure

    External sphincter Voluntary,Responsible for pressure on voluntarysqueeze

    Innervated by somatic nerves

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    Gall bladder

    Concentrates bile and works as reservoir

    Empties in relation to meals in response tohormones

    Sphincter of Oddi several parts HPZ

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    Pancreas

    1. Exocrine function

    2. Secretion of HCO3

    3. Endocrine function Insulin, Glucagon,

    Somatostatin Hormonal mechanisms for regulation

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    Physiology of Swallowing

    1. Oral stage tongue voluntary control

    2. Pharyngeal stage Reflex

    Food stimulates swallow receptors

    Swallow centre inhibits respiration

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    3. Oesophageal stage

    Peristalsis + Gravity

    7-10 sec

    LES pressure 20mmHg over intra-gastricpressure at rest

    Pressures equal during swallowing

    LES opens until bolus and contractionhave passed through

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    Factors affecting LES Pressure

    Increase Gastrin, Motilin, Vasopressin

    Protein

    Prokinetics

    Decrease Proges.,Secretin,CCK,Glucagon

    Fat, alcohol, chocolate

    Ca blockers, Benzodiazepines,Theophylline, Atropine

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    Disorders of Swallowing

    1. Mechanical eg. Ca, FB

    2. Neuromuscular incoordination eg.Achalasia, DES, Bulbar palsy

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    Achalasia

    Autoimmune/ Genetic/ Infective

    Loss of ganglion cells in myenteric plexus

    Degenerative changes in vagus & DMN

    Chagas is aquired achalasia

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    Manometry in Achalasia

    Absence of peristalsis

    Elevated LES pressure

    Incomplete relaxation of LES

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    GERD

    Gastric acid pH 1.5 2

    Oesophageal pH 6 7

    Physiological reflux After meals, shortduration, not during sleep

    Pathological reflux long duration, D/N,symptomatic

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    Aetiology of GERD

    1. Incompetent LES

    2. Deficient/delayed acid clearance

    3. Gastric abnormalities

    4. Transient LES relaxation

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    Incompetent LES

    1. Hormonal factors eg. Progesterone inpregnancy

    2. Length of LES exposed to higherintragastric pressure Hiatus hernia

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    Delayed acid clearance

    1. Primary peristalsis D/N = 60/6

    2. Secondary peristalsis absence ofswallow

    3. Salivation neutralises acid

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    Gastric abnormalities

    1. GOO

    2. Delayed emptying eg. DM, vagotomy

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    Basis of tests

    Manometry LES pressure & length

    24 hr oesophageal pH Quantify,frequency, timing

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    Physiology of defaecation

    Distension of rectum registered in cortex

    RAIR IAS relaxes

    Faeces in contact with upper anal receptors Receptors determine quality and content

    (sampling reflex)

    Contraction of rectum, relaxation of EAS,pelvic floor & puborectalis sling

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    Anorectal Manometry

    Resting pressure autonomic neuropathy,MDA

    Squeeze pressure Trauma, surgery

    RAIR absent in Hirshprungs

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