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ANATOMY & PHYSIOLOGY OF THE BOWEL Gill Nottidge Continence Nurse Specialist.

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Presentation on theme: "ANATOMY & PHYSIOLOGY OF THE BOWEL Gill Nottidge Continence Nurse Specialist."— Presentation transcript:

1 ANATOMY & PHYSIOLOGY OF THE BOWEL Gill Nottidge Continence Nurse Specialist

2 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

3 Digestion period  Stomach:  3hours – converted to chyme  Small intestine:  4 – 6 hours  Large intestine:  12 – 72 hours

4 5 Main functions of the bowel 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 Small intestine Duodenum 12 ins Jejunum 5-8 feet Ileum feet Goblet cells in the mucosa produce mucus. The duodenum is the major portion of the small intestine where enzyme secretion takes place.

6 Small intestine Absorptive surface in adults 7600cm Lined with villi to increase surface area 90% of our daily fluid intake is absorbed in the small intestine

7 Large intestine 5-6 feet in length Caecum with appendix Ascending colon Transverse colon Descending colon Sigmoid colon

8 Structure of intestine Small & large intestine has 4 layers Peritoneal Muscular Submucosal Mucosal

9 Peristalsis 2-3 mass peristaltic movements per day Stimulated by consumption of food and warm drinks

10 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


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14 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)

15 Normal Defaecation 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

16 Correct position

17 Bristol Stool Chart

18 What affects the bowel? Poor diet Lack of fluid Mobility Medications Surgery

19 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

20 Effect of endocrine system Pancreas – Diabetes Adrenal glands – fight/flight Corticotrophin-releasing factor (CRF) – (Stress hormone) eg. IBS

21 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)

22 Reflexes Anal wink Anal reflex Perineal reflex Reflexive contraction of external anal sphincter on touching/stimulation

23 WHAT IS AUTONOMIC 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

24 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

25 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

26 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)

27 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

28 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)

29 Constipation!

30 Thank you for your attention. Any questions? Gill Nottidge Tel:




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