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ANATOMY & PHYSIOLOGY OF THE BOWEL Gill Nottidge Continence Nurse Specialist. CC01 Assess bladder and bowel dysfunction.
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ANATOMY & PHYSIOLOGY OF THE BOWEL Gill Nottidge Continence Nurse Specialist
CC01 Assess bladder and bowel dysfunction • an in-depth understanding of the anatomy and physiology of the male and female lower gastro intestinal tract in relation to lower bowel function and continence status including: • a) stool production and what influences this • b) normal defaecation • c) the nervous system including autonomic dysreflexia • d) the bowel • e) the pelvic floor/complex and anal sphincter muscles • f) the endocrine system • g) reflexes
Digestion period • Stomach: • 3hours – converted to chyme • Small intestine: • 4 – 6 hours • Large intestine: • 12 – 72 hours
Absorption – Minerals, water, fats, medicines Secretion – Enzymes secreted by the small intestine Mucus secreted by the colon to help lubricate the faeces Synthesis – Synthesises some vitamins Storage – unabsorbed food residue Elimination – Propulsion of faecal matter and absorption of fluid 5 Main functions of the bowel
Small intestine • Duodenum 12 ins • Jejunum 5-8 feet • Ileum 16-20 feet • Goblet cells in the mucosa produce mucus. • The duodenum is the major portion of the small intestine where enzyme secretion takes place.
Absorptive surface in adults 7600cm Lined with villi to increase surface area 90% of our daily fluid intake is absorbed in the small intestine Small intestine
Large intestine • 5-6 feet in length • Caecum with appendix • Ascending colon • Transverse colon • Descending colon • Sigmoid colon
Structure of intestine • Small & large intestine has 4 layers • Peritoneal • Muscular • Submucosal • Mucosal
2-3 mass peristaltic movements per day Stimulated by consumption of food and warm drinks Peristalsis
Excretion • How does it work? • Muscles work together to propel waste matter (Peristalsis) • During process substances not absorbed by the body becomes faeces • Faeces arrives in rectum to be expelled
Pelvic floor muscles • Supports the pelvic organs • Contraction causes urethral compression – helps maintain continence during abdominal pressure • Collectively called “Levator Ani” • Striated muscle slow and fast • muscle fibres (under Voluntary control)
Full rectum Adopt correct posture Raise intra-abdominal pressure Internal and external anal sphincters relax Rectum contracts to expel stool Should pass soft formed stool with minimal effort Sphincter “snaps shut” after completion “Normal” 3 times / day to 3 times / week Normal Defaecation
What affects the bowel? • Poor diet • Lack of fluid • Mobility • Medications • Surgery
Continence is Complex • Anal sphincters (structural integrity, residual function if damaged) Internal anal sphincter - passive stool retention External anal sphincter- control of urge to stool • Pelvic floor and mucosal seal • Sensory function and co-ordination • Stool consistency (e.g. diet) • Gut motility • Emotional factors • Lifestyle and toilet access
Effect of endocrine system • Pancreas – Diabetes • Adrenal glands – fight/flight • Corticotrophin-releasing factor (CRF) – (Stress hormone) eg. IBS
Nervous system • Vagus nerves – stimulate acid secretion • Intestine – sympathetic and parasympathetic nerve supply - sub mucosa • Internal sphincter – autonomic (smooth muscle) • External sphincter – under voluntary control (striated muscle)
Reflexes • Anal wink • Anal reflex • Perineal reflex • Reflexive contraction of external anal sphincter on touching/stimulation
WHAT ISAUTONOMIC DYSREFLEXIA? • It develops after spinal cord injury/ lesion at or above T6 • Exaggerated response of nervous system to localised trigger below level of spinal cord injury • This causes an sudden extreme rise in blood pressure • It can occur without warning and is a medical emergency
Autonomic Dysreflexia • Normally a harmful stimulus causes the autonomic nervous system to respond resulting in a rise in blood pressure. • If T6 lesion or above present, stimulus below the injury causes BP to rise, but autonomic nervous system does not act to lower it below the lesion. • Therefore BP continues to rise until stimulus is removed • Autonomic nervous system attempts to lower BP above lesion: this causes the symptoms that aid the diagnosis of AD
Signs and symptoms • Stuffy nose / nasal obstruction • Severe pounding headache, usually frontal • Raised BP (by 20mm/hg) / bradycardia • Cutis anserina (goose bumps) above and possibly below level of SCI and shivering • Flushing above level of lesion due to vasodilatation • Reduced urine output • Blurring vision – spots before eyes • Increased spasms
What Goes Wrong? • Anal sphincter (childbirth, injury, iatrogenic damage, degeneration) Internal - passive soiling; External - urge incontinence • Gut motility (infection, inflammation, radiation, hypermotility, emotions) • Stool consistency (diet, motility, anxiety)
What Goes Wrong? • Local pathology (prolapse, piles, fistula) • Neurological damage (motor or sensory) • Lifestyle, toilets, drugs, immobility, frailty • Impaction with “overflow diarrhoea” most common in frail dependent individuals
Facts • Annual spend on laxatives in the UK is £50 million per year. (DH 2001) • The UK has the highest incidence of bowel cancer in the world with 20,000 new cases per year • One in three people consulting GPs have a bowel problem • Bowel disorders such as irritable bowel syndrome, colitis, crohns disease and diverticulitus affect 1:250 people in the UK (National association for colitis and crohn’s disease 2010)
Thank you for your attention. Any questions? Gill Nottidge Tel: 01274 322210 Gillian.nottidge@bradford.nhs.uk