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Life Maintenance > Week 11 - GI tract > Flashcards

Week 11 - GI tract Flashcards

1
Q

What do we produce to support digestive process throughout GI tract? and approx how much?

A

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

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2
Q

What is absorbed in the small intestine? List is at goes down (11)

A

Water soluble vitamins (active) Fat soluble vitamins (passive through micelles) Ca, Fe, Zn Polysaccharides, proteins and fats Magnesium Bile acids Vitamin B12

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3
Q

What gets absorbed by the colon? (4)

A

Na, Cl, H2O, small chain fatty acids

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4
Q

Why do people get diarrhoea? (4 categories)

A

Osmotic (non-absorbable solute) Secretory (impaired electrolyte transport) Exudative (intestinal mucosal damage) Motility (increased transit)

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5
Q

Types/causes of osmotic diarrhoea (4)

A

Deficiency in digestive enzymes Lactulose Magnesium salts sorbitol

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6
Q

Types/causes of secretory diarrhoea (4)

A

Bacterial endotoxins Bile salts Laxatives Hormone producing tumours

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7
Q

Types/causes of exudative diarrhoea (6)

A

Infections IBD Coeliac diseaase Irradiation Ischaemia Colon cancer

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8
Q

Types/causes of motility diarrhoea (4)

A

Irritable bowel syndrome Thyrotoxicosis Autonomic neuropathy (DM) drugs

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9
Q

Different phases of malabsorption (what are they and describe what may be going wrong) (3)

A

Luminal phase - reduced nutrient availability, impaired fat solubility, defective nutrient hydrolysis Mucosal phase Transport phase

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10
Q

Consider questions you may ask when taking patient history for diarrhoea

A

Time course / severity Impact of food, fasting Volume / consistency of stool Floating , bloody stool Nocturnal symptoms? Weight loss, fever, vomiting?

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11
Q

Investigations of diarhhoea

A

Blood tests Stool tests Functional tests Imaging Endoscopy Gut hormone profile Urinary catecholamines

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12
Q

What is IBS?

A

Functional GI disorder - a disorder of gut-brain interaction Very common group of disorders related to the gut

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13
Q

What is coeliac disease?

A

Inflammatory condition of small intestinal muscosa, improves on removal of gluten from diet Inherited auto-immune condition

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14
Q

Treatment of coeliac disease

A

Gluten exclusion Dietary supplements Information and support from PAGs

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15
Q

Follow up following coeliac diagnosis

A

6 monthly OPA (repeat small intestinal biopsy after 1st 6 months) blood tests symptomatic assessment nutritional assessment dietary compliance & close monitoring during pregnancy

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16
Q

Management of poor response / relapse of coeliac disease

A

Dietary compliance correct diagnosis? Other co-incident disease?

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17
Q

Importance of adhering to gluten free diet following coeliac diagnosis

A

Amelioration of symptoms reduction in risk of osteoporosis reduction in risk of associated malignancies reduction in risk of associated autoimmune diseases

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18
Q

What is IBD?

A

chronic, relapsing, immunologically mediated disorders that are collectively referred to as IBD

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19
Q

What is ulcerative colitis?

A

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)

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20
Q

What is Crohn’s disease?

A

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)

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21
Q

Complications of Crohn’s disease

A

Stricture - resulting in lack of bowel movements, vomiting, pain

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22
Q

Epidemiology of UC vs Crohn’s (numbers, men/women/age)

A

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

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23
Q

Relationship between smoking and IBD

A

Appears protective against UC (but not long term) Makes Crohn’s worse

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24
Q

Appendicectomy and IBD

A

Appears protective against UC (not Crohn’s)

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25
Q

Presentation of UC vs Crohns

A

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)

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26
Q

What are the extra-intestinal manifestations of IBD?

A

EYES - Episcleritis, Uveitis Mouth - Stomatitis, ulcers Liver - steatosis Biliary tract - gallstones,

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27
Q

What are the musculoskeletal complications with IBD?

A

Arthritis - more common in Crohn’s Osteoporosis - due to steroid use and reduced physical activity

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28
Q

Dermatological manifestations of IBD

A

Erythema nodosum, pyoderma gangrenosum (don’t operate because it will show up wherever you operate)

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29
Q

Hepato-biliary manifestations of IBD

A

Primary sclerising cholengitis, cholelithiasis, portal vein thrombosis, drug-induced hepatotoxcity or pancreatitis, gallstones

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30
Q

What does lack of bile acid absorption cause?

A

Irritation of large intestine (if not absorbed in illeum, it moves into cecum and irritates it causing diarrhoea)

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31
Q

Where is B12 absrobed

A

Terminal ileum

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32
Q

Treatment for UC (6)

A

5-Amino-salicylates Azathioprine Oral steroids Intravenous hydrocortisone Ciclosporin (uncommon) Infliximab

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33
Q

How do you diagnosis severe colitis?

A

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

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34
Q

What does the parasympathetic nervous system regulate in the eye? (3)

A

pupil diameter, intra-ocular pressure, accommodation (focusing)

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35
Q

Sympathetic response in bladder

A

Relaxes smooth muscle, B2 (allows bladder to hold more urine) Contracts internal sphincter (holds urine in)

36
Q

Parasympathetic response in bladder

A

Contracts smooth muscle to move urine out of bladder, M3 receptors

37
Q

Motor response in bladder

A

Skeletal muscle controls external sphincter (Nic receptors), contraction and relaxing

38
Q

In parasympathetic nervous system, what is generally role of M3 receptors?

A

Contract smooth muscle

39
Q

What is ‘crisis’ approach or labelling theory?

A

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

40
Q

What is primary and secondary deviance?

A

Primary - illness as a deviation from norm Secondary - behaviour change following diagnosis Disease becomes self-fulfilling prophecy

41
Q

Experience of stigma with chronic illness (two types)

A

Enacted stigma - discriminatory experiences from societal reaction Felt stigma - Change to person’s self-identity based on ‘imagined’ social reaction

42
Q

Describe the negotiation model

A

Experience of chronic disease has ups and downs (‘dynamic and temporal’) - experience of labels and stigmas may shift over time, constant struggle

43
Q

Outcomes of randomised control trials (endpoint, primary, secondary)

A

Endpoint: Primary:

44
Q

What is the value of random allocation? (3)

A

Eliminates allocation bias Minimises confounding Facilitates blinding

45
Q

What is the role of the placebo? (3)

A

Ensures blinding Minimises assessor bias Minimises response bias

46
Q

What is allocation bias?

A

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)

47
Q

What is ascertainment bias?

A

Response bias (participants) and assessment bias (researchers)

48
Q

Components of treatment and placebo responses

A

BOTH have placebo effect and natural epidemiology Treatment response also has treatment effect

49
Q

What is natural epidemiology?

A

Outcome without treatment or observation

50
Q

What is the Hawthorne effect?

A

Behavioural change as motivational response to interest, care, attention received from observation and assessment

51
Q

How do you calculate the actual pharmaceutical effect?

A

Total effect minus the placebo and natural epidemiology to understand what the active treatment itself is likely actually doing

52
Q

Describe difference between placebo response and placebo effect (same for treatment response and effect)

A

Placebo response is the observed outcome for the placebo group Placebo effect is the psychological response that occurs across ALL treatment groups

53
Q

Extraintestinal features of UC (7)

A

General: anaemia, fever Hepatobiliary: primary sclerosing cholangitis Eye: Uveitis Joints: Ankylosing spondylitis & sacro-ileitis Skin: Pyoderma gangrenosum

54
Q

Extraintestinal features of Crohns (8)

A

General: anaemia, fever Oropharynx: aphthous ulcers Eye: Anterior uveitis Joints: Seronegative arthritis Skin: Erythema nodosum Perineum: Anal skin tags & perineal fistulae

55
Q

Short term risks of UC (2)

A

anaemia toxic megacolon, perforation and peritonitis

56
Q

Short term risks of Crohn’s (3)

A

intestinal obstruction fistulae pericolic abscess

57
Q

Long term risks of UC

A

adenocarcinoma of colon: risk proportional to length of colon involved, length of history and duration of active disease

58
Q

Long term risks of Crohn’s

A

increased risk of adenocarcinoma of colon and small bowel lymphoma

59
Q

Examples of GI conditions in childhood (5)

A

Gastroeosophageal reflux Chronic constipation Gastroenteritis Coeliac disease IBD

60
Q

Prevalence of gastrooesophageal reflux in 4 months old

A

67%, most often will spontaneously stop (only 1% still have symptoms at 1 year)

61
Q

What are the tests for GOR in infants

A

Common to do no investigation as will likely resolve on its own Gold standard is 24hr pH monitor May do endoscopy

62
Q

Treatment of GOR infants

A

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

63
Q

Describe coeliac disease presenting in childhood

A

Growth and/or delayed puberty Bone demineralisation, fractures miserable, fretting Dental enamel abnormalities

64
Q

Diagnostic criteria for coeliac disease in children and adults (5)

A

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

65
Q

Issues, signs of IBD in children (4)

A

Nutritional status and growth delay Sexual maturation delay Psychological adjustments Low compliance with therapy

66
Q

Psychological considerations with IBD in children/adolescents

A

Separation anxiety Body image Privacy Sexuality Autonomy

67
Q

Often the first presentation of childhood Crohn’s

A

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

68
Q

Determining whether recurrent abdominal pain is psychological (4)

A

Greater than 3 months Interferes with normal activities Usually periumbilical No other underlying pathology

69
Q

Encopresis

A

Passage of faeces in inappropriate places

70
Q

Symptoms of constipation in children

A

Abdominal pain, distension, discomfort Poor appetite, lack of energy Mood change Painful defecation (which can turn into withholding behaviours)

71
Q

Hirschsprungs

A

Lack of innervation in rectum (sometimes more widely)

72
Q

Describe pernicious anaemia

A

Autoimune disorder Gastric parietal cell antibodies and intrinsic factor antibodies Causes lack of intrinsic factor and lac of B12 absorption

73
Q

Role of B12 and Foods containing B12

A

Role - essential co-factor for methylation in DNA and cell metabolism Fish, meat dairy, marmite

74
Q

Role of folate and foods containing folate

A

Role - DNA synthesis, adenosine, guanine and thymidine synthesis Dark green leafy vegetables, fruits, nuts, beans, avocado, spinach, etc. Some countries fortify flour

75
Q

Why can someone be iron deficient? (2 with examples)

A

Not enough in - poor diet, malabsorption, increased need Losing too much - blood loss, menstruation, GI tract loss, parasites

76
Q

How do you measure iron?

A

Serum Fe (highly variable during day) Ferritin - primary storage protein Tranferrin saturation (looks at ratio of serum iron and total iron binding capacity)

77
Q

Where is iron absorbed? What type of receptors?

A

Duodenum and proximal jejunum Ferroportin receptor

78
Q

Why do we need iron?

A

Essential for O2 transport, erythropoeisis

79
Q

Signs of iron deficiency before anaemia (6)

A

angular stomatitis, oesophageal stricture, fatigue, hair loss, mental function (unfocused), skin changes

80
Q

Where is iron stored? Can it be free?

A

Special cells need to store iron (macrophages, Kupffer cells in liver), free iron is toxic

81
Q

What happens if there is too much iron?

A

Hemochromatosis (opposite of iron deficiency), results in end organ damage (heart, thyroid, pancreas)

82
Q

Path of iron within the body

A

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

83
Q

What regulates iron levels in the body / movement from storage?

A

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

84
Q

What are the three overarching reasons you may have reduced haemoglobin?

A

Failure of production Failure of appropriate utilisation Increased destruction

85
Q

What may cause short lifespan of RBC?

A

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

86
Q

How does malaria affect RBCs?

A

Malaria causes haemolysis (as does osmotic instability, membrane disorders such as hereditary spherocytosis)

87
Q

What do RBCs have within them?

A

Hb Mitochondria NO NUCLEUS - except if released early which makes you wonder if something wrong with spleen

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