Acute Abdomen + Physiology Flashcards
How is GI function regulated?
Integration of neural and hormonal signals Neurohormonal control: integration of neural + hormonal signals
Outline the 3 neural stages of digestion.
a) Cephalic (30%): Sight, smell, thought or taste
• Stimuli ≈ neurogenic signals ≈ cerebral cortex ≈ medulla oblongata + appetite centres of amygdala and hypothalamus ≈ dorsal motor nuclei of vagus nerve ≈ vagus nerve to stomach = Meissner’s (Submucosal plexus) + Auerbach’s (myenteric) plexus ≈ ACh ≈ intramural gastric neurons ≈ ACh ≈ M3r of Parietal cells (fundus) ≈ HCl secretion + Motility (from submucosal and mucosal plexus)
b) Gastric (60%): Stretch (distension) + Raised pH
• Stimuli ≈ stretch receptors + chemoreceptors ≈ enteric NS + peptides and AAs ≈ ENS efferents and GRP neurone efferents ≈ ACh release + Gastrin ≈ Parietal cells to increase more HCl + ECL cell increase HA which increases parietal cell HCl + G cells to secrete more gastrin ≈ Increased acid secretion and motility
c) Intestinal (10%): Acid and semi-digested fats ≈ enterogastric reflex
• Stimuli ≈ inhibitory signals to the
i) Stomach by enteric NS
ii) Medulla by afferent neurones to inhibit vagal nuclei
iii) Chyme stimulates S and I cells of duodenum to release secretin and CCK which stimulate pancreas and gall bladder, acinar cells produce enzymes and suppress gastric secretion and motility
Outline the Cephalic stage of digestion.
a) Cephalic (30%): Sight, smell, thought or taste
• Stimuli ≈ neurogenic signals ≈ cerebral cortex ≈ medulla oblongata + appetite centres of amygdala and hypothalamus ≈ dorsal motor nuclei of vagus nerve ≈ vagus nerve to stomach = Meissner’s (Submucosal plexus) + Auerbach’s (myenteric) plexus ≈ ACh ≈ intramural gastric neurons ≈ ACh ≈ M3r of Parietal cells (fundus) ≈ HCl secretion + Motility (from submucosal and mucosal plexus)
Outline the Gastric phase of digestion.
b) Gastric (60%): Stretch (distension) + Raised pH
• Stimuli ≈ stretch receptors + chemoreceptors ≈ enteric NS + peptides and AAs ≈ ENS efferents and GRP neurone efferents ≈ ACh release + Gastrin ≈ Parietal cells to increase more HCl + ECL cell increase HA which increases parietal cell HCl + G cells to secrete more gastrin ≈ Increased acid secretion and motility
Outline the Intestinal phase of digestion.
c) Intestinal (10%): Acid and semi-digested fats ≈ enterogastric reflex
• Stimuli ≈ inhibitory signals to the
i) Stomach by enteric NS
ii) Medulla by afferent neurones to inhibit vagal nuclei
iii) Chyme stimulates S and I cells of duodenum to release secretin and CCK which stimulate pancreas and gall bladder, acinar cells produce enzymes and suppress gastric secretion and motility
List 3 main hormonal regulators of digestive function. State the specific site of production for each.
a) Gastrin: Enteroendocrine G cells in gastric mucosa (Pyloric Glands in Pyloric antrum)
b) Secretin: Enteroendocrine S cells in gastric mucosa (Duodenum)
c) CCK: Enteroendocrine I cells in duodenum releasing CCK in response to FAs and small peptides
d) GIP: Produced by enteroendocrine K cells in response to glucose in SI
State the site of production and functions of Gastrin.
Gastrin: Enteroendocrine G cells in gastric mucosa (Pyloric Glands in Pyloric antrum)
• gastric acid secretion from parietal cells
• Peristalsis (GI motility via smooth muscle contraction)
• Relax pyloric sphincter (≈ gastric emptying
State the site of production and functions of Secretin.
Secretin: Enteroendocrine S cells in gastric mucosa (Duodenum)
• [HCO3-] secretion by pancreas ≈ stabilise chyme pH
• Bile production by liver
• Reduced GI motility (reduced contraction of smooth muscle and GI mucosa)
State the site of production and functions of CCK.
CCK: Enteroendocrine I cells in duodenum releasing CCK in response to FAs and small peptides
• [HCO3-] secretion by pancreas
• Secretion of pancreatic enzymes
• Contraction of gallbladder + relaxation of Sphincter of Oddi ≈ flow of bile into duodenum
• Inhibition of gastric emptying
• Growth of exocrine pancreas
State the site of production and functions of GIP.
d) GIP: Produced by enteroendocrine K cells in response to glucose in SI
• Stimulates pancreas to release insulin
Which hormone is responsible for the contraction of the gallbladder and relaxation of the Sphincter of Oddi?
CCK
State two hormones which inhibit gastric emptying.
Secretin
CCK
Are the timings of the three regulatory phases of GI function discrete?
No, there is considerable temporal overlap between the three regulatory phases of GI function
What is salivary secretion?
Addition of substances (fluids, ions and enzymes) into lumen of GI tract from salivary glands
State 3 substances which are present in salivary secretion. For each, give a factor which increases these or decreases.
Bicarbonate: PSNS (inc.) cf Sleep/Dehydration/Atropine (dec.)
K+: PSNS cf Sleep/Dehydration/Atropine
Amylase: SNS cf Sleep/Dehydration/Atropine
Lingual lipase: SNS cf Sleep/dehydration/atropine
What is the process of HCl secretion from the parietal cell?
Stimuli (Gastrin, HA, ACh, distension and peptides) bind CSR (GPCR or L-AA transporter) ≈ rise in IC Ca++ or cAMP ≈ secretion mediated by proton pump P5 (Na/K ATPase) which transports cations in opposite directions under physiological function to create electrochemical gradient as K+ IN and H+ OUT. When stimulated, large changes occur and vesicles which possess p+ pumps become active and translocate from cytosol to apical membrane and fuse together to increase surface area
What is the innervation of the exocrine component of the pancreas?
ANS follows Rest and Digest
- PSNS from vagus ≈ increased secretion
- SNS from Coeliac + SM ganglia ≈ reduced secretion
Outline the duct system of the exocrine pancreas regarding its functioning.
The exocrine compartment of the pancreas is composed of a duct system with berry-like acinar cells connected by intercalated ducts that drain into intralobular collecting ducts and subsequently into the main pancreatic duct. The pancreatic duct runs the entire length of the pancreas and unites with the common bile duct at the Hepatopancreatic Ampulla of Vater, which drains into the duodenum at the major duodenal papilla
What is the regulation of salivary secretion?
1) PSNS: Stimuli (+/-) —> chemo-/mechanoreceptors —> Afferent nerve impulses (+/- cerebral cortex prior to integration) —> Salivary centre in medulla —> CNVII and CN IX —> ACh —> M3 (Gaq) —> IP3, Ca++ ≈ secretion ≈ saliva ≈ large volume, watery + enzyme rich (serous; parotid)
2) SNS: Stimuli (+) —> chemo-/mechanoreceptors —> Afferent nerve impulses (+/- cerebral cortex prior to integration) —> salivary centre in medulla —> T1-T3 —> NE —> ß1 (Gas) —> cAMP ≈ secretion ≈ saliva which is mucous rich, small volume and thick (sublingual gland)
What are salivation reflexes?
List two different types of salivation reflex and outline their pathway.
1) Simple (unconditioned): Food (stimulus) —> chemoreceptors/mechanoreceptors in mouth —> afferent nerves —> salivary centre in medulla —> impulses via autonomic nerves (SNS + PSNS stimulation) —> Salivary glands increase production
2) Acquired (conditioned): Sight/thought/smell —> Afferent impulses along afferent nerves —> Cerebral cortex —> Salivary centre in medulla —> impulses via autonomic nerves (SNS + PSNS stimulation) —> Salivary glands increase production
What are the stages of salivation and where are these mediated?
1) Acini cells: 1º secretion which is isotonic
• Ions: Na+, Cl-, K+, HCO3-
• Enzymes: Amylase and mucin production
2) Myoepithelial cells: Eject saliva into ductal cells from acini cells
• Saliva into ducts
3) Duct cells: 2º secretion + modification
• Ions: Reabsorb Na+ and Cl-; add K+; Alter HCO3- according to flow rate (proportional association)
• High flow rate ≈ increased [HCO3-] ≈ osmotic gain drawing more water in
• Low flow rate ≈ reduced [HCO3-]
List 5 substances secreted from the stomach.
HCl
Pepsinogen
Intrinsic factor
Mucous
Gastrin
Somatostatin
Regarding HCl, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
Parietal Cell in Oxyntic Gland
Protein degradation + Pepsinogen activation @ pH2
Increase: Thought/smell Distension ACh HA PSNS Gastrin
Decrease: Ghrelin Acidity (low pH) Chyme in duodenum SS Atropine Ranitidine Omeprazole
Regarding Intrinsic Factor, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
Parietal Cell (Oxyntic Gland)
Vitamin B12 absorption
Inc. Thought/smell Distension ACh HA PSNS
Dec. Ghrelin Acidity (low pH) Chyme in duodenum SS Atropine Ranitidine Omeprazole
Regarding pepsinogen, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
Mucous Neck Cell (Oxyntic)
Chief Cells (Oxyntic)
Proenzyme cleaved to form pepsin
Inc. Thought/smell Distension ACh HA PSNS
Dec. Ghrelin Acidity (low pH) Chyme in duodenum SS Atropine Ranitidine Omeprazole
Regarding Mucous, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
MNCs (Oxyntic)
Lubrication + barrier
Inc. Thought/smell Distension ACh HA PSNS
Dec. Ghrelin Acidity (low pH) Chyme in duodenum SS Atropine Ranitidine Omeprazole
Regarding Gastrin, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
G cell (Pyloric)
Stimulate digestion via: HCl from parietal cells, pyloric sphincter relax and hepatic bile production
Inc. Thought/smell Distension ACh HA PSNS
Dec. Ghrelin Acidity (low pH) Chyme in duodenum SS Atropine Opiates
Regarding Somatostatin, what is its site of production, role and list 3 factors which increase and 3 which decrease its secretion from the stomach.
D cells (Oxyntic + Pyloric)
Inhibit parietal cell acid secretion
Inc.
Acidity
Chyme in duodenum
VIP from Vagus
Dec. Thought/smell Distension ACh HA PSNS
What is secreted from the pancreas?
High [HCO3-]
Enzymes: Pancreatic lipase, pancreatic amylase and pancreatic protease
List factors which increase or decrease pancreatic secretion.
Inc.
Secretin
CCK
PSNS
Dec.
Ghrelin
Opiates
What is the formation of pancreatic secretions regarding fluid and enzymes and how is this formed?
Stimulation by the physiological agonists CCK (I cells of duodenum) and ACh (Vagal nerve stimulation) cause an elevation of intracellular calcium which activates the calcium-activated chloride channel in the apical membrane, leading to fluid secretion
Outline the molecular mechanism of secretion by a pancreatic acinar and ductal cell.
i) (ACh): Vagal nerve efferents —> ACh —> M3r (GPCR) —> PLC —> IP3 —> IP3r2 and IP3r3 on ER —> Channel opens —> Ca++ elevation —>
a) Ductal cells: Open Cl- channel (TMEM16A) in apical membrane —> Na+ paracellular transport through tight junctions —> NaCl in lumen generates osmotic gradient —> water efflux via apical AQP5 water channels
b) Acinar cells: binds with synaptotagmin 2 (calcium sensor) for synchronised exocytosis (of vesicles containing enzymes)
ii) (CCK): Duodenal I cells —> CCK —> CCK1r —> indirectly open RyR on ER membrane —> Channel opens —> Ca++ elevation —>
a) Ductal cells: Open Cl- channel (TMEM16A) in apical membrane —> Na+ paracellular transport through tight junctions —> water efflux via apical AQP5 water channels
b) Acinar cells: binds with synaptotagmin 2 (calcium sensor) for synchronised exocytosis (of vesicles containing enzymes)
List 3 pancreatic enzymes.
- Pancreatic amylase
- Pancreatic lipase
- Pancreatic protease
List 5 components of bile. Give 3 stimuli for bile secretion.
Components:
Bile Salts
Bile Pigments (Bilirubin)
Cholesterol Esters
Phospholipids
HCO3-
Stimuli:
Secretin (production)
CCK (contraction of GB and relaxation of SOD)
Central and enteric neural input
What is bile?
Mixture of bile salts, bile pigments, cholesterol esters and bicarbonate which is produced by hepatocytes and stored in gallbladder, is not enzymatic, and emulsifies fats into micelles to prepare for digestion and solubilise products of digestion into micelles
What is the LI?
digestive organ which is partly intraperitoneal (transverse) and partly retroperitoneal (ascending and descending) which secretes alkaline mucous, protecting and lubricating the large bowel and responsive for absorption of vitamins
What is the secretory function of the LI?
Stimuli (distension, VIP and ACh increase secretion cf Adrenaline and SS reduce secretion)
1) Alkaline mucous ≈ protection + lubrication + neutralisation of H+ from gut bacteria - High K+ - High HCO3-
List the sequence of mechanical digestion.
1) Mastication
2) Deglutition
3) Storage
4) Mechanica digestion
5) SI movements
6) Colon movements
Outline the chewing reflex.
Chewing reflex = Bolus of food in mouth —> inhibition of mastication ≈ jaw drops ≈ stretch reflex of jaw muscles —> afferent feedback —> Nuclei in brainstem —> CN V —> mastication ≈ rebound contraction ≈ incisors cut + molars grind to increase SA
Outline deglutition. Give the two stages.
Bolus at posterior of pharynx —> epithelial swallowing receptors —> afferent neurone CN V + CN IX —> medulla oblongata —> efferent motor impulses via CN V, CN IX + CN X—> elevation + retraction of velum (soft palate) ≈ velopharyngeal closure + palatopharyngeal folds medial (sagittal selection slit) —> larynx + epiglottis lifted upwards ≈ prevent choking/asphyxiation + upper oesophageal sphincter opens —> pharyngeal muscles contract ≈ 1º +/- 2º peristaltic wave (2º if vagus afferent fibres detect food —> MO —> CN IX + CN X ≈ 2º peristaltic contraction)
Stages:
• Oropharyngeal phase (Oral phase + Oral transmit phase + Pharyngeal phase)
• Oesophageal phase (1º and 2º peristaltic wave)
Outline the process of storage in the stomach.
Food enters stomach via upper oesophageal sphincter (cardiac sphincter) —> stretch/distension —> afferent feedback via CN X —> Medulla oblongata —> reduce tone in muscle wall ≈ rugae distend + increase volume (vasovagal reflex)
• Vasovagal reflex
Outline the process and 3 key areas of mechanical digestion.
Weak peristaltic mixing waves —> Constrictor rings of increasing intensity —> Retropulsion —> Chyme (food + stomach secretions)
Three stages
• Weak peristaltic mixing waves: Food in stomach —> distension —> vagal afferents; myenteric plexus —> MO; interneurone —> vagal efferents; myenteric plexus efferent —> weak peristaltic constrictor waves (mixing waves) in upper portion of stomach
• Retropulsion: Weak peristaltic constrictor (mixing) waves in upper portion of stomach —> increase intensity ≈ constrictor rings forcing antral contents under high pressure towards pylorus —> pylorus muscle contracts to prevent emptying via pylorus ≈ upstream squeezing ≈ retropulsion
• Pyloric pump: antral peristaltic contractions —> pyloric sphincter relaxes (modulated by nervous + hormonal signals) —> chyme passes into the duodenum
Outline the SI movements. State the main reflex of this stage.
(mixing contraction + propulsive contraction however less distinct as all movements cause a mixture of both contraction type)
• Segment contractions: Distended with chyme —> local concentric contractions along intestine —> segmentation of small intestine (spaced segments) with varied frequency of slow waves determined by intrinsic slow waves in smooth muscle + intrinsic ENS
• Peristaltic waves: Chyme propelled through SI by peristaltic waves with net movement
• Gastroileal reflex: Intensifies peristalsis in ileum forcing chyme through ileocaecal valve (ileocaecal valve controlled by SNS ganglia or myenteric plexus in gut wall)
• Reflex: Gastroileal reflex
Outline the key colon movements and reflexes.
Haustrations (circular + longitudinal muscle contractions) —> mass movements (modified peristalsis with constrictive ring at point of distension in colon then lose haustration and contract as unit propelling faecal material further down colon) —> Defaecation
• Haustrations: Circular muscle contract ≈ constrict lumen + longitudinal muscle contract (teniae coli) ≈ elongate lumen sagittally
• Mass movements: Modified peristalsis ≈ constrictive ring at point of distension + distal to constrictive ring loss of haustration ≈ propel faecal material down colon without interruption
• Gastrocolic + Duodenocolic reflexes: distension of stomach/duodenum —> enteric nervous system —> increase colonic motility + mass movements
• Defaecation: Defaecation reflex whereby facets enter rectum —> local enteric nervous system triggered (myenteric plexus in Submucosa) —> peristalsis in descending colon, sigmoid and rectum —> inhibitory signals from myenteric plexus (rest and digest) + PSNS augment intrinsic myenteric defaecation (increase motility + relax internal anal sphincter ≈ parasympathetic defaecation reflex) ≈ internal anal sphincter relaxed + external anal sphincter consciously relaxes
- Gastrocolic reflex
- Duodenocolic reflex
- Defaecation reflex
Give two inhibitory reflexes which are not directly from the GI tract and may cause inhibition and why does this occur?
1) Peritoneointestinal reflex: Peritoneum irritation strongly inhibiting excitatory enteric nerves ≈ intestinal paralysis due to peritonitis
2) Renointestinal/vesicointestinal reflexes: Kidney or Bladder irritation strongly inhibiting excitatory enteric nerves ≈ intestinal paralysis due to kidney or bladder infection
What factors modulate SI peristalsis and how?
Increase SI peristalsis: - Duodenal distension - Gastroenteric reflex (distension of stomach conducted via myenteric plexus along to SI) - Gastrin - CCK - Insulin - Serotonin - Motilin
Decrease SI peristalsis:
- Secretin
- Glucagon
What factors alter gastric emptying?
Increase gastric emptying:
- Increased food volume in stomach: distension ≈ increase peristalsis (weak + constrictor rings) ≈ increase pyloric pump
- Gastrin: increase peristalsis, gastric acid secretion and relax pyloric sphincter ≈ gastric emptying
Decrease gastric emptying: Enterogastric reflex from duodenum via ENS, SNS (increase impulses) or PSNS (reduce impulses) - Distension of duodenum - Irritation of duodenum - Acidity of duodenal chyme - Breakdown products: FAs and Proteins - CCK: block increased stomach motility - GIP: reduce GI motility - Secretin: reduce GI motility
List the factors which may contribute to the development of malnutrition in IBD?
1) Reduced dietary intake
2) Altered energy/nutrient metabolism
3) Increased GI nutrient losses
4) Drug-nutrient interactions
What are the manifestations of malnutrition in IBD?
1) Protein Energy Malnutrition (PEM)
- UC > CD
2) Altered body composition
- ∆ composition due to pro-inflammatory cascade + drugs e.g. steroids ≈ weight gain/adiposity + changed lifestyle such as reduced sport ≈ ∆ body composition
3) Micronutrient deficiencies
- Poor absorption + diarrhoea
- Vitamins A, B, C, D, E and Minerals Zn, Se, Cu, Ca++ \
4) Poor bone health
- Reduced bone mineralisation due to drugs (steroids), low activity (reduced PA) and reduced intake (low micronutrients) and metabolism (pro-inflammatory cytokines on bone formation, resorption and osteoblast maturation)
5) Reduced linear growth
- Shorter height due to poor bone growth and soft tissues
List the main micronutrient deficiencies a patient with IBD is vulnerable to.
- Fe
- Folic Acid
- Selenium
- Zinc
- Calcium
- Vitamin A - Vitamin B12 (cobalamin)
- Vitamin B1 (thiamine) - Vitamin B6 (pyridoxine)
- Vitamin D
- Vitamin K
Why may IBD patients have a higher risk of low bone density, osteoporosis and fractures?
1) Inflammation
2) Steroids
3) Reduced physical activity
4) Malabsorption
What are the calcium requirements for adult patients with IBD and how do they differ to the general adult population? State where this can come from.
1000mg per day for IBD patients cf adults require 700mg per day;
- Milk
- Cheese
- Yoghurt
- Custard
- Fortified juice
- Sardines
- Scampi
- Pitta bread/chapatti
Give a screening tool which can be used to assess nutrition in a patient with IBD.
Malnutrition Universal Screening Tool (MUST) is a validated screening tool comprising of 5 steps which is scored from 0-6.
Step 1: BMI calculation
0-2 (18.5-20 5 days
Step 4: Calculate
Step 5: Stratification
0 = low risk (repeat annually community or weekly hospital)
1 = medium risk (document intake for 3 days; hospital weekly and community 2-3 months)
2 = high risk (refer to dietitian, nutritional support team; set goals and monitor/review care plan weekly in hospital and monthly in community)
When is artificial nutrition support recommended for a patient?
Enteral tube feeding (delivery of nutritionally complete feed via tube into stomach, duodenum or jejunum)
Consider enteral tube feeding in patients who are at risk of malnutrition or malnourished and have inadequate/unsafe oral intake and functional, accessible GI tract
What may the benefit of enteral nutrition in Active CD be?
Exclusive enteral nutrition believed to promote mucosal healing in GI tract by positively altering intestinal microbiota, reducing intestinal permeability and promoting reduction in inflammatory cytokines
For which patient group is enteral nutrition often the primary therapy for inducing remission in active Crohn’s Disease and why?
Primary therapy for induing remission in active Crohn’s Disease supported in CD especially in children where adverse consequences f steroid therapy are proportionally greater, impacting nutrition, immune system and MSK growth
When might enteral nutrition be used in adults with active Crohn’s Disease to induce remission?
Acute active CD +/- may be susceptible to steroid treatment
Is enteral nutrition as a primary therapy for inducing remission in UC indicated?
Primary therapy using nutrition to treat IBD not supported in UC
What is a food-reintroduction diet?
Structured dietary protocols designed to slowly add food back to diet after period of exclusive enteral nutrition e.g. LOFFLEX ≈ exclude all foods which may cause food intolerance and followed for 2-4 weeks
What is Coeliac Disease?
Autoimmune disease associated with chronic inflammation of SI with malabsorption of glutens leading to malabsorption of micro and macronutrients increasing risk of complications
When should testing for Coeliac disease be considered in adults and children? Describe the recommended diagnostic process?
Serological tests should be offered to patients with:
- Persistent unexplained abdominal or GI symptoms
- Faltering growth
- Prolonged fatigue
- Unexpected weight loss
- Severe or persistent mouth ulcers
- Unexplained iron, vitamin B12 or folate deficiency
- Type 1 Diabetes
- Autoimmune thyroid disease
- Irritable Bowel Syndrome
- First degree relative with Coeliac Disease
List the foods that should be excluded from the diet by someone who has been diagnosed with Coeliac Disease and consider the implications of excluding gluten-containing foods from diet both practically and nutritionally?
Avoid gluten for life, gluten-free diet which can be found online (coeliac.org.uk) - Barley - Bulgar wheat - Couscous - Durum wheat - Flours made from wheat, rye or barley - Porridge oats, oat milk - Biscuits and breads - Muesli, wheat based breakfast cereals - Canned and dried fresh wheat noodles and pasta - Meat and poultry cooked in batter or breadcrumbs - Beer, lager, stout
List foods that someone with Coeliac Disease can safely include in their diet and using Eatwell Guide consider how someone with Coeliac Disease can continue to consume a varied, balanced diet.
- Meat - Fish - Fruit and vegetables - Rice - Potatoes - Lentils - Fruit juice - Flavoured water - Fizzy drinks - Cider - Wine - Sherry - Spirits - Port
Would a patient with Coeliac Disease need to take supplements? What are the RDI for calcium and vitamin D?
Take vitamin D and calcium supplements if dietary intake insufficient
Vitamin D: 10mcg
Calcium: 700mcg
What dermatological condition may accompany Coeliac Disease?
Dermatitis Herpetiformis, skin lesion which comprises of erythematous, pruritic excoriations consisting of urticarial plaques, papules with vesicles on the elbows, knees, buttocks, lower back and scalp appearing in older patients (50-69 years)
What is Irritable Bowel Syndrome?
Chronic, relapsing and remitting lifelong disorder featuring abdominal pain associated with defaecation and change in bowel habit
What first-line dietary advice would you give to a patient with IBS?
- Regular meals
- Avoid missing meals
- 8 cups of fluid
- Restrict caffeinated drinks to 3 per day
- Limit intake of high-fibre food - Reduce intake of resistant starch
- Limit fruit to 3 portions per day
- Avoid Sorbitol (artificial sweetener) if diarrhoea (osmotic diarrhoea)
What lifestyle factors may be discussed with a newly diagnosed IBS patient?
Lifestyle - Stress management - Leisure time and relaxation time - Physical activity - Symptom targeted medication
List the complications of Coeliac Disease.
Osteoporosis Ulcerative jejunitis Malignancy Functional hyposplenism Vitamin D deficiency Iron deficiency
What are the 4 major functions of the GI tract?
- Secretion (7L)
- Absorption (8.9L)
- Motility
- Digestion
Where are salivary secretions derived from/secreted by? How may these be classified?
1) Sublingual
• Floor of mouth
• Beneath tongue
• Mucous gland: Mucous-rich
2) Submandibular
• Inferior to mandibular lower edge
• Mixed glands: serous + mucous cells ≈ seromucous gland
3) Parotid
• Inferior to ear and over masseter (jaw muscle)
• Serous gland: Serous secretion ≈ aqueous fluid of water, ions and enzymes
What is oesophageal peristalsis?
1º peristaltic wave from beginning to end of oesophagus taking 4-10 seconds pushing food to stomach with circular fibres squeeze bolus down and longitudinal fibres shorten distance of travel
- Circular + Longitudinal muscle fibres
- Water travels faster
- Sticky food may get lodges ≈ 2º peristaltic wave + increased saliva production
- Food enters stomach through lower oesophageal sphincter (cardiac sphincter)
