Week 11 - GI tract Flashcards
What do we produce to support digestive process throughout GI tract? and approx how much?
Salivary amylase (.5L/day) In stomach, HCl =, IF, pepsinogen, gastrin (2L/day) Gallbladder releases bile (0.9L/day) Pancreas releases HCo3, amylase, lipase, tripsinogen (0.6L/day) Small intestine release disaccharidases, peptidases, somatostatin (1.8L/day) TOTAL SECRETIONS 5.8L/day
What is absorbed in the small intestine? List is at goes down (11)
Water soluble vitamins (active) Fat soluble vitamins (passive through micelles) Ca, Fe, Zn Polysaccharides, proteins and fats Magnesium Bile acids Vitamin B12
What gets absorbed by the colon? (4)
Na, Cl, H2O, small chain fatty acids
Why do people get diarrhoea? (4 categories)
Osmotic (non-absorbable solute) Secretory (impaired electrolyte transport) Exudative (intestinal mucosal damage) Motility (increased transit)
Types/causes of osmotic diarrhoea (4)
Deficiency in digestive enzymes Lactulose Magnesium salts sorbitol
Types/causes of secretory diarrhoea (4)
Bacterial endotoxins Bile salts Laxatives Hormone producing tumours
Types/causes of exudative diarrhoea (6)
Infections IBD Coeliac diseaase Irradiation Ischaemia Colon cancer
Types/causes of motility diarrhoea (4)
Irritable bowel syndrome Thyrotoxicosis Autonomic neuropathy (DM) drugs
Different phases of malabsorption (what are they and describe what may be going wrong) (3)
Luminal phase - reduced nutrient availability, impaired fat solubility, defective nutrient hydrolysis Mucosal phase Transport phase
Consider questions you may ask when taking patient history for diarrhoea
Time course / severity Impact of food, fasting Volume / consistency of stool Floating , bloody stool Nocturnal symptoms? Weight loss, fever, vomiting?
Investigations of diarhhoea
Blood tests Stool tests Functional tests Imaging Endoscopy Gut hormone profile Urinary catecholamines
What is IBS?
Functional GI disorder - a disorder of gut-brain interaction Very common group of disorders related to the gut
What is coeliac disease?
Inflammatory condition of small intestinal muscosa, improves on removal of gluten from diet Inherited auto-immune condition
Treatment of coeliac disease
Gluten exclusion Dietary supplements Information and support from PAGs
Follow up following coeliac diagnosis
6 monthly OPA (repeat small intestinal biopsy after 1st 6 months) blood tests symptomatic assessment nutritional assessment dietary compliance & close monitoring during pregnancy
Management of poor response / relapse of coeliac disease
Dietary compliance correct diagnosis? Other co-incident disease?
Importance of adhering to gluten free diet following coeliac diagnosis
Amelioration of symptoms reduction in risk of osteoporosis reduction in risk of associated malignancies reduction in risk of associated autoimmune diseases
What is IBD?
chronic, relapsing, immunologically mediated disorders that are collectively referred to as IBD
What is ulcerative colitis?
Only affects colon Diarrhoea with blood and mucus Exacerbation and remissions Proctitis - just the rectum (urgency) Left sided colitis - descending colon only (some risk of perforation) Pancolitis - all large intestine (larger risk of perforation)
What is Crohn’s disease?
Chronic granulomatous inflmmatory disease ANY part of GI tract from mouth to anus Commonest site is ileo-colonic (last bit of small, first bit of large)
Complications of Crohn’s disease
Stricture - resulting in lack of bowel movements, vomiting, pain
Epidemiology of UC vs Crohn’s (numbers, men/women/age)
UC 11/100,000, Equal men and women Crohn’s 7/100,000. a bit more in women (2% more) Same age range - 15-30, 60-80
Relationship between smoking and IBD
Appears protective against UC (but not long term) Makes Crohn’s worse
Appendicectomy and IBD
Appears protective against UC (not Crohn’s)
Presentation of UC vs Crohns
UC - blood diarrhoea, mucus, mucosal and submucosal, continuous disease (all bowel affected) Crohns - Abdominal pain, diarrhoea, abdominal mass (may present with swinging fevers), fistulas/strictures, perianal disease, rectal sparing, skip lesions (patchy)
What are the extra-intestinal manifestations of IBD?
EYES - Episcleritis, Uveitis Mouth - Stomatitis, ulcers Liver - steatosis Biliary tract - gallstones,
What are the musculoskeletal complications with IBD?
Arthritis - more common in Crohn’s Osteoporosis - due to steroid use and reduced physical activity
Dermatological manifestations of IBD
Erythema nodosum, pyoderma gangrenosum (don’t operate because it will show up wherever you operate)
Hepato-biliary manifestations of IBD
Primary sclerising cholengitis, cholelithiasis, portal vein thrombosis, drug-induced hepatotoxcity or pancreatitis, gallstones
What does lack of bile acid absorption cause?
Irritation of large intestine (if not absorbed in illeum, it moves into cecum and irritates it causing diarrhoea)
Where is B12 absrobed
Terminal ileum
Treatment for UC (6)
5-Amino-salicylates Azathioprine Oral steroids Intravenous hydrocortisone Ciclosporin (uncommon) Infliximab
How do you diagnosis severe colitis?
Truelove and Witts criteria 6+ bloody stools daily + one or more of: Temp over 37.8 Pulse over 90 Haem less than 10.5 ESR over 30
What does the parasympathetic nervous system regulate in the eye? (3)
pupil diameter, intra-ocular pressure, accommodation (focusing)
Sympathetic response in bladder
Relaxes smooth muscle, B2 (allows bladder to hold more urine) Contracts internal sphincter (holds urine in)
Parasympathetic response in bladder
Contracts smooth muscle to move urine out of bladder, M3 receptors
Motor response in bladder
Skeletal muscle controls external sphincter (Nic receptors), contraction and relaxing
In parasympathetic nervous system, what is generally role of M3 receptors?
Contract smooth muscle
What is ‘crisis’ approach or labelling theory?
Focuses on societal reaction to your chronic illness (rather than the actual physical impact) Chronic irreversibly changes status of the individual (‘labelled’) - your diagnosis is a label you can’t remove
What is primary and secondary deviance?
Primary - illness as a deviation from norm Secondary - behaviour change following diagnosis Disease becomes self-fulfilling prophecy
Experience of stigma with chronic illness (two types)
Enacted stigma - discriminatory experiences from societal reaction Felt stigma - Change to person’s self-identity based on ‘imagined’ social reaction
Describe the negotiation model
Experience of chronic disease has ups and downs (‘dynamic and temporal’) - experience of labels and stigmas may shift over time, constant struggle
Outcomes of randomised control trials (endpoint, primary, secondary)
Endpoint: Primary:
What is the value of random allocation? (3)
Eliminates allocation bias Minimises confounding Facilitates blinding
What is the role of the placebo? (3)
Ensures blinding Minimises assessor bias Minimises response bias
What is allocation bias?
Participants allocated to different groups based on characteristic - subconscious or nor (not the same as selection bias, which refers to taking particular sample from population)
What is ascertainment bias?
Response bias (participants) and assessment bias (researchers)
Components of treatment and placebo responses
BOTH have placebo effect and natural epidemiology Treatment response also has treatment effect
What is natural epidemiology?
Outcome without treatment or observation
What is the Hawthorne effect?
Behavioural change as motivational response to interest, care, attention received from observation and assessment
How do you calculate the actual pharmaceutical effect?
Total effect minus the placebo and natural epidemiology to understand what the active treatment itself is likely actually doing
Describe difference between placebo response and placebo effect (same for treatment response and effect)
Placebo response is the observed outcome for the placebo group Placebo effect is the psychological response that occurs across ALL treatment groups
Extraintestinal features of UC (7)
General: anaemia, fever Hepatobiliary: primary sclerosing cholangitis Eye: Uveitis Joints: Ankylosing spondylitis & sacro-ileitis Skin: Pyoderma gangrenosum
Extraintestinal features of Crohns (8)
General: anaemia, fever Oropharynx: aphthous ulcers Eye: Anterior uveitis Joints: Seronegative arthritis Skin: Erythema nodosum Perineum: Anal skin tags & perineal fistulae
Short term risks of UC (2)
anaemia toxic megacolon, perforation and peritonitis
Short term risks of Crohn’s (3)
intestinal obstruction fistulae pericolic abscess
Long term risks of UC
adenocarcinoma of colon: risk proportional to length of colon involved, length of history and duration of active disease
Long term risks of Crohn’s
increased risk of adenocarcinoma of colon and small bowel lymphoma
Examples of GI conditions in childhood (5)
Gastroeosophageal reflux Chronic constipation Gastroenteritis Coeliac disease IBD
Prevalence of gastrooesophageal reflux in 4 months old
67%, most often will spontaneously stop (only 1% still have symptoms at 1 year)
What are the tests for GOR in infants
Common to do no investigation as will likely resolve on its own Gold standard is 24hr pH monitor May do endoscopy
Treatment of GOR infants
Reassurance Milk thickening agents Feeding advice - little and often May give acid suppressing drugs (PPI) - but shouldn’t have to give meds in th e first year of life
Describe coeliac disease presenting in childhood
Growth and/or delayed puberty Bone demineralisation, fractures miserable, fretting Dental enamel abnormalities
Diagnostic criteria for coeliac disease in children and adults (5)
Tissue transglutaminase titres > x10 upper limit of normal If not 10x higher, EMA and then biopsy Clinical response on GFD good test (but not for asymptomatic patients) Gluten challenge
Issues, signs of IBD in children (4)
Nutritional status and growth delay Sexual maturation delay Psychological adjustments Low compliance with therapy
Psychological considerations with IBD in children/adolescents
Separation anxiety Body image Privacy Sexuality Autonomy
Often the first presentation of childhood Crohn’s
Growth failure (sometimes without any GI symptoms or before GI symptoms) Steroids can suppress growth, but they can reduce inflammation - balance and try to take off after 3 months max
Determining whether recurrent abdominal pain is psychological (4)
Greater than 3 months Interferes with normal activities Usually periumbilical No other underlying pathology
Encopresis
Passage of faeces in inappropriate places
Symptoms of constipation in children
Abdominal pain, distension, discomfort Poor appetite, lack of energy Mood change Painful defecation (which can turn into withholding behaviours)
Hirschsprungs
Lack of innervation in rectum (sometimes more widely)
Describe pernicious anaemia
Autoimune disorder Gastric parietal cell antibodies and intrinsic factor antibodies Causes lack of intrinsic factor and lac of B12 absorption
Role of B12 and Foods containing B12
Role - essential co-factor for methylation in DNA and cell metabolism Fish, meat dairy, marmite
Role of folate and foods containing folate
Role - DNA synthesis, adenosine, guanine and thymidine synthesis Dark green leafy vegetables, fruits, nuts, beans, avocado, spinach, etc. Some countries fortify flour
Why can someone be iron deficient? (2 with examples)
Not enough in - poor diet, malabsorption, increased need Losing too much - blood loss, menstruation, GI tract loss, parasites
How do you measure iron?
Serum Fe (highly variable during day) Ferritin - primary storage protein Tranferrin saturation (looks at ratio of serum iron and total iron binding capacity)
Where is iron absorbed? What type of receptors?
Duodenum and proximal jejunum Ferroportin receptor
Why do we need iron?
Essential for O2 transport, erythropoeisis
Signs of iron deficiency before anaemia (6)
angular stomatitis, oesophageal stricture, fatigue, hair loss, mental function (unfocused), skin changes
Where is iron stored? Can it be free?
Special cells need to store iron (macrophages, Kupffer cells in liver), free iron is toxic
What happens if there is too much iron?
Hemochromatosis (opposite of iron deficiency), results in end organ damage (heart, thyroid, pancreas)
Path of iron within the body
Iron in absorbed by enterocytes in the gut, transferred by transferrin to liver, storage cells to store as ferritin, moved to bone marrow to make blood when needed
What regulates iron levels in the body / movement from storage?
Regulated by hepcytin - helps to absorb iron from gut, release iron from stores (through negative feedback process) Also switched on by inflammation/infection Hepsidin is for iron, as insulin is for glucose
What are the three overarching reasons you may have reduced haemoglobin?
Failure of production Failure of appropriate utilisation Increased destruction
What may cause short lifespan of RBC?
early breakdown / desctruction, Metabolic causes sickle cell, thalassaemia, malaria Malaria causes haemolysis (as does osmotic instability, membrane disorders such as hereditary spherocytosis) Destruction - mechanic heart valve or any rough surface (vasculitis, narrow valve), immune destruction
How does malaria affect RBCs?
Malaria causes haemolysis (as does osmotic instability, membrane disorders such as hereditary spherocytosis)
What do RBCs have within them?
Hb Mitochondria NO NUCLEUS - except if released early which makes you wonder if something wrong with spleen
