Unit 10; Crohns, coeliac, lactose intolerance and colitis

Question 1

What are some common causes of diahorrea?

Answer 1

Infections/food posioning
Antibiots - affect microbiome - risk of opportunistic pathogens
Medication side effect
Allergies (milk, fruits)
Stress and anxiety
Dietary factors
Travelers diarrhoea - acute, caused by infections typically E.coli and norovirus

Question 2

What are the different classifications of chronic diahorrea?

Answer 2

Osmotic
Secretory
Inflammatory
Abnormal GI motility

Question 3

How can diarrhoea be classified by time span?

Answer 3

Acute - less than 14days
Persistent: more than 14 days
Chronic: more than 4 weeks

Question 4

What dietary foods increase the risk of diarrhoea?

Answer 4

Caffeine - activates Type 2 Bitter receptors in the oral cavity, increase gastrin and CCK, increases acid production and colon peristalsis
High insoluble fibre - wheat, nuts, beans and vegetables - osmotic diahorrea

Question 5

What is diarrhoea?

Answer 5

A decrease in faecal consistency (increased fluidity), stools that cause urgency or abdominal discomfort or increase in frequency of stool (typically more than 3 times a day)

Question 6

What is meant by osmotic diarrhoea?

Answer 6

Hypertonic fluid in the colon increases water secretion from the ECF by osmosis, down a water potential gradient
Due to malabsoprtion or osmotically active substances in the intestinal lumen, typically high salts such as MgSo4 used as a laxative

Question 7

What is secretory diahorrea?

Answer 7

Copious secretion in the small intestine, the colon does not have the capacity yo reabsorb excessive water
Usually caused by infectious agents

Question 8

What is gut motility diarrhoea?

Answer 8

Increased gut motility, water and electrolytes deliverd and passed to the colon too fast for water to be absorbed
Associted with parasitic infections such as Giardia

Question 9

What is inflammatory diarrhoea?

Answer 9

Most commonly caused by IBD, less common include opportunistic infections such as TB.
More prevalent in patients who are immune compromised.
Fecal calprotectin is often used as a biomaker

Question 10

What are the effects of stress on the GI?

Answer 10

1.Comfort eating - hedonic eating
2.Stress diarrhoea - increased motility of the colon
3.Cortisol can increase appetite, stimulate the lateral nucleus in the hypothalamus
4.Trophic effect of cortisol due to directed blood flow from the GIT - decreases GI motility, mucosa degenerates and enzyme production decreases (can lead to constipation)
5. Increases gastric acid and pepsin secretion
6. Altered microbiome - dysbiosis can increase the risk of inflammation and infection

Question 11

What are the effects of diet on the GI system?

Answer 11

1. Effect on microbiome: high plant fibres, low in fat and protein is beneficial, pro and prebiotics
2. Diarrhoea and constipation risk: soluble v insoluble fibre, caffeine, high salt diet
3. Alcohol - negative effect on the liver.
4. Raw foods or undercooked foods - risk of food poisoning, bacterial infections
5. Fizzy drinks, caffeine, alcohol - increase gastric acid secretion

Question 12

What is the mechanism of action of loperamide?

Answer 12

Used for symptomatic treatment for acute diarrhoea, chronic dairrhoea and faecal incontinence - is available over the counter - is not recommended in children

Eneteric nuerons synthesise and release opioid peptides and neurotransmitters.
loperamide bind to mu-opiod receptor on circular and longitudinal muscle, and acts as agonist – this recruits G protein receptors kinases and activates downstream signalling that inhibits enteric nerve activity, particularly reduces Ach and prostaglandins.

Decrease peristalsis and fluid secretion in the GIT, increases transit time, increase rectal tone, increased tone of the anal sphincter, inhibits fluid and ion secretion
= leads to reduced daily decal volume and increased viscosity and bulk of feces, decreased urgency

Effects last from within 1 hour to 3 days

Question 13

What treatments can be used as anti-diarrhoeal drugs?

Answer 13

1.Antibiotics - acute infection caused inflammatory diarrea - may use ciproflaxin
2.Opiods - codeine, loperamide hydrocholride
3. Muscarininc receptor antagonists -such as atropine
4. Oral rehydration therapy

Question 14

What happens in order to initiate the defecation reflex?

Answer 14

Ingestion of food triggers to gastrocolic reflex - mediated by gut hormones and stretch receptors in the stomach - results in increased motility/peristalisis in the colon
Moves digestive content from the colon into the rectum
Distention is detected by stretch receptors in the colon
This triggers the defecation reflex

Question 15

What are the different defecation reflexes?

Answer 15

Intrinsic reflex
Parasympathetic reflex/ extrinsic reflex

Question 16

What happens during the intrinsic reflex of the defecation reflex?

Answer 16

Local enteric nervous system in the rectal wall
Myenteric plexus initiates peristalsis in the colon and rectum towards the anus
This reflex is often weak and needs to be fortified to cause a bowel movement

Question 17

What happens during the parasympathetic defecation reflex?

Answer 17

Rectum stretch receptors activates nerve endings
This is relayed to the spinal cord then back out via parasympathetic fibres in the pelvci nerves
This intensifies peristalsis and relaxation of the internal anal sphincter
More effective in large bowel movements

Question 18

What is the role of conscious control int eh defecation reflex?

Answer 18

Somatic nerve - the pudendal nerve - from the conscious cortex allows relaxation of the external anal sphincter, the puborectalis muscle and the pelvic floor
This allows defecation when it is socially convenient

Question 19

What is lactose intolerance?

Answer 19

Arises due to lactase deficiency.
Lactase normally breaks lactose down into glucose and galactose.
When non-functional lactose builds up in the small intestine
Lactose is fermented by bacteria in the gut: this produces glucose, glactose, H2, Co2 and methane
Some gases are exhaled or absorbed, others remain in the tissue causing bloating
Lactose build up also increases osmolarity of the colon - lead to osmotic diarrhoea

Question 20

How does the hydrogen breath test identify lactose intolerance?

Answer 20

1.Breath sample collected and tested for hydrogen
2. A solution of lactose (25g to 50g is given to drink
3. Breath samples are taken into a bag with a syringe attached and recorded at intervals to monitor for hydrogen production, normally take at least 10 samples
4. An increase by >220ppm over baseline indicates lactose malabsoprtion - and potential bacterial overgrowth

Question 21

What is the ethnic link to lactose intolerance?

Answer 21

More common in Asian and south African ethnicities, particularly China
THought to be due to low dairy content in ancestoral diet (cow diseases or lack of cattle)
Western ethnicites evolved to maintain lactase after weaning in order to digest milk in diet (Lactase retainment)
Whilst in asian ethnicicities this was not needed so more likely to loose lactase during weening and not have a functional lactase as an adult causing lactose intolerance.

Question 22

What is the meant by irritable bowel syndrome?

Answer 22

Functional disorder - change in the functioning of systems that than disease affecting the structure of the body
Diagnosis is based on ruling out other causative diseases
Does not involved inflammation or damage to the GIT - no detectable structural abnormalities

Question 23

What is the potential pathology of IBS? Irritable bowel syndrome

Answer 23

Altered gut motility - increased intraluminal pressure, disorders peristalsis.
Visceral hypersensitivity to distention
Altered brain gut axis
Stress - exaccerabte only
Nreve endings in bowel are considered sensitive and nerves that control muscles are unusually active

Question 24

What symptoms are normally associated with IBS?

Answer 24

Continuously or recurrently for 3 months: abdominal pain relieved by defaecation, change in stool frequency and consistently
Supporting symptoms include: mucorrhoea and abdominal bloating.

Question 25

Why might an Irritable Bowel syndomre diagnosis be considered milder than an INflammatory Bowel disease?

Answer 25

IBS - does not increase risk of colon cancer, IBD does

IBS - typically require less hospitalisation and surgery is very rare.

Question 26

What is the hereditary link to inflammatory Bowel disease?

Answer 26

NOD2 gene - loss of function
IL-23R gene - gain of function
TNFSF15 - gain of function, regulates immune homeostatise, resulting in increased INFy and NK responses
alpha4beta7 - increased function on inflammatory T cell phnoetypes

Question 27

How is a NOD2 mutation linked to inflammatory bowel disease?

Answer 27

is an intracellular PPR found in epithelial cells in the gut , loss of function, unable to recognise bacteria, results in bacterial persitance and chronic inflammation

Question 28

How is the IL23R gene linked to Inflammatory bowel disease?

Answer 28

Gain of function mutation
IL-23 released by macrophages, promotes development of Th17 - enhances neutrophil response.
Cascade signalling it increased inflammatory response such as TNFalpha release, and NK cell activation.

Question 29

What is the pathophysiology of crohns disease?

Answer 29

1.Predisposition due to genetic and environmental factors
2.Onset thought to be triggered by dysbiosis of the gut microbiome
IMMUNE RESPONSE:
APC - presents antigen - activation of Th1 - cytokines release - activation of macrophages - increases platelet-activating factor, proteases and free radicals. Activation of IEL killing infected epithelial cells.
3.Impaired NOD2 ability leads to persistence of the pathogen, and reduced effectiveness of macrophages, paneth cells and dendritic cells. Leads to chronic inflammation
Impaired autophagy leading to failure to kill bacteria
4. Reduced barrier integrity allows pathogens to invade into the lamina propia and encourages further dysbiosis.
By this stage there is activation of the innate and adaptive immune response
5. Increase in pro-inflammatory cytokines in response to impaired bacterial clearance. Characteristics Th17 effector responses
6. Uncontrolled immune response damaging the bowel indicates IBD

Question 30

What type of disease is crohns disease?

Answer 30

An inflammatory bowel disease characterised by an immune-mediated cause.

Question 31

What are the key histological features of ulcerative colitis?

Answer 31

Inflammation in the mucosa (lamina propria) and submucosa
Ulceration of the mucosa
Mild fibrosis

Question 32

What are the key histological features of Crohn’s disease?

Answer 32

Transmural inflammation
Granuloma
Fistula
Stricture
Fissuring Ulceration - skip lesions
Significant fibrosis

Question 33

Why is there a tendency for gastric ulcers in the pylorus and cardia?

Answer 33

Contains majority of mucus glands
Damaged mucus glands - significantly decrease mucus production
Increased exposure of tissue that is less adapted to acidic environment to stomach acid resulting in ulceration

Question 34

What immune cell type is normally found in crohns and UC?

Answer 34

Lymphocytes

Question 35

What are the key pathological features of crohns disease?

Answer 35

Crypt distoration
Fissuring ulceration (skip lesion)
Mural hyperplasia
Lymphoid aggregates
Granuloma
Inflammatory infiltrate from mucosa to muscularis external (tranmucosal inflammation)
Fat wrapping

Question 36

What are the key patholiglca features of ulcerative colitis?

Answer 36

Ulceration - mucosa maybe into submucosa
Pseudopolyps _ due to ulceration
Crypt abscess
Inflammatory infiltrate into submucosa

Question 37

What is the difference in teh location of crohns disease and ulcerative colitis?

Answer 37

Crohns - mouth to anus, 60% have anal involvement
UC - Continuous inflammation, normally beginning in the rectum and spreading to the sigmoid colon. 20% have anal involvement

Question 38

What are the differences in teh potential future complications from Crohns disease and UC?

Answer 38

Crohns - fat and vitamin malabsoprtion, strictures and fistulas are more likely, more fibrosis and serositis, malignant change is less common than UC

UC - malignant change is more common, no malabsorption, very mild fibrosis and serostitis if any

Question 39

How is ANCA used in diagnosis of IBD?

Answer 39

Not rasied in Crohns
Raised in Ulcerative colitis
ANCA is an antibody that may be produced in an autoimmune condition, typically target protein inside white blood cells mainly neutrophils
Tested for immunoassay

Anti-neutrophil cytoplasmic antibodies.

Question 40

How does the risk of smoking vary between crohns and ulcerative colitis?

Answer 40

Crohns - increased risk
Ulcerative collitis - protective factor

Question 41

What are some blood biomarkers of inflammation?

Answer 41

CRP - activate complement
ESR - increased in inflammation, due to increased pro-coagulatn factors
Procalcitonin - indicates systemic inflammation

Question 42

What are some faecal biomarkers of inflammation and what do they indicate?

Answer 42

Calprotectin - calcium binding protein found in neutrophil cytoplasm
Lactoferrin - iron binding glycoprotein secretes in neutrophil secondary granules

Question 43

What signs on physical examination are indicative of crohns disease?

Answer 43

Weight loss, malnutrition
Apthous ulceration of the mouth - inflammatory or nutritional deficiency
Angular chelitisis - vitamin A deficiency.
Occosional abdominal tenderness and right illiac fossa mass (sticture build up of faeces and fibrous and mural hyperplasia

Question 44

What is responsible for the cobblestone appearance in crohns disease>

Answer 44

Skip lesions
And deep longitudinal ulcers

Question 45

How does small bowel imaging help diagnose Crohns disease?

Answer 45

Barium meal follow through - appears white
Bubble warp appearance - cobblestone mucosa
Fistulas and strictures can also be idneitifed by considering the flow of barium and the width of the lumen

Question 46

What is the pathophysiology process of ulcerative colitis?

Answer 46

Combination of environmental and genetic factors.
Autoimmune conditions - thought to be triggered by molecular mimicry, where immune response launched against a pathogen with a similar antigen structure to those found in neutrophils
Is characterised by CD8+ cells
Also triggered by bacteria producing large amounts of sulfides
Produce p-ANCA and c-ANA targes proteins found in neutrophils

Question 47

Symptoms of Crohn’s disease

Answer 47

Pain - right lower quadrant
Diarrhoea
Blood in stool from ulceration
Malabsoprtion - present as anemia or ulcers in the corners of the mouths weight loss
Bloating and fever - due to presence of bacteria
Anal involvement - pain or drainge

Question 48

symptoms of ulcerative colitis

Answer 48

Pain - lower left quadrant
Diarrhoea
Blood in stool
Unintended weight loss - diahorrea, drugs, or reduced appetite

Question 49

What types of anemia are common in IBD?
What are the causes?

Answer 49

Pernicious anemia - crohns damage to the terminal ileum, vitamin B12 and IF complex is unable to bind to IFR

Iron deficiency anemia - malabsorption due to damage to the duodenum including DMT1 receptors

Blood loss (hemolytic anemia) - reduced levels of rbcs and Hb in the blood stream

Question 50

What is the mechanism of action of prednisolone

Answer 50

Is a glucocorticoid - has a cholsesterol base as a steroid
Pass through cell membrane into the cytoplasm where it binds to glucocorticoid receptors, which are actived when they heterodimerise and dissocited from heat shock proteins
Binds to glucocorticoid response element in the nucleus, acts as a transcription factor to alter gene expression
Results in increased expression of anti-inflammatory cytokines such as TGF-beta and reduced expression of pro-inflammatory cytokines such as TNFalpha
Can induce apoptosis in TNFalpha dependent immune cells such as lymphocytes.
Reduces capillary permeability and migration of lymphocytes.
increases Annexin A1 transcription - which inhibits COX-2 and and PLA2 - prevents prostaglandin production

Overall leads to a chemical and cellular profile that favours anti-inflammatory conditions.

Question 51

What are the side effects of prednisolone?

Answer 51

**Cushing syndrome - moon face (round and red), slow growth rate and weight gain with fat accumulation on the trunk but loss from the arms, legs and buttocks.

Commonly causes:
*Anxiety, behaviour abnormality and cognitive impairment
Electrolyte imbalance and fluid retention
*GIT discomfort
Fatigue, nausea, osteoporosis, skin reactions and sleep disorders hypertension

Lots of high risk side effects

Question 52

Give some examples of immunosuppressant drugs used in crohns

Answer 52

Mercaptopurine
Methotrexate
Vedolizumab
Adalimumab

Question 53

Mercaptopurine MOA (immunsuppresant)

Answer 53

Is taken up by t-lymphocytes, decreases NFKb causing apoptosis of leukocytes, is converted into TIMP, TIMP inhibits processed involving IMP meaning purine bases are not synthesised. Converted into TGTP which is inserted into RNA preventing elongation during transcription. Finally is converted into TdGTP which is inserted into DNA inhibiting semi-conservative replication. This inhibits the S phase of the cell cycle. Hence it can be used as an immunosuppresant or a cancer (ALL) maintenance therapy.

Question 54

Methotrexate MOA (immunsuppresant)

Answer 54

Prevents the proliferation of inflammatory cells by antagonising the production of folate.
Is an antimetabolite, folic analogue. It does this by inhibiting the dihydrofolate reductase enzyme (thymine synthesis), inhibits AICART (purine synthesis), decreasing AICART also has anti-inflammatory effects. This prevents the formation of new DNA nucleotides, this stops the cell cycle during interphase. This stops the proliferation of immune
cells.

Question 55

Vedolizumab MOA in crohns disease

Answer 55

Monoclonal antibody, binds specifically to alpha 4 beta 7 dextrin, prevents from binding to MaDCAM-1 found in endothelial cells in the GIT
To prevent gut homing of memory T lymphocytes into GALT
Causes a reduction in gastrointestinal inflammation.

Question 56

Adalimumab MOA in crohns disease

Answer 56

Is a monoclonal antibody. Is anti-inflammatory, binds to TNF alpha, and prevents interaction with cell surface receptors p55 and p75 on immune cells (not Rbcs or immature T cells).
This decreases pro-inflammatory cytokine secretion, leukocyte migration, decreases epidermal thickness, causes apoptosis in mononuclear cells with TNF alpha receptors, and inhibits the release of IL-6 and acute-phase proteins. Used in Crohn’s disease and arthritis.

Question 57

What is the recommended treatment plant for inducing remission in a patient with crohns disease?

Answer 57

1. Glucorticoids - prednisolone most often
2. If not avaiable consider budesonide or amniosalicylates
3. If severe and active may consider biological therapies such as adalimuman and vedolizumab

Question 58

Aminosalicylates MOA

Answer 58

Member of the drug class includes sulfasalazine
Split into acitve components by bacteria in the gut: 5-ASA and sulfapyridine
5-ASA remains in lumen, is absorbed, acts on nuclear receptor
Signalling pathway alters gene expression to decrease expression of NFKB and COX-2 this reduced pro-inflammatory cytokines

Question 59

How are Crohn disease flare ups managed?

Answer 59

1. Conventional glucocorticoids if first flare up in 12 months
2. Otherwise suggest addition of mercapopurine, azathioprine or methotrexate

Question 60

How do you maintain remission i Crohns disease?

Answer 60

Encourage regular surveilence of the colon
Mercaptopurine and methotrexate
No glucocorticoid treatments

Question 61

What is the aim of Crohn’s disease treatment?

Answer 61

Induce and maintain remission
Achieve mucosal healing to prevent disease progression and complications

Question 62

How might the treatment of crohns disease vary based on severity? (NOT related to NICE guidelines)

Answer 62

Mild - 5-ASA, may add antibiotics if uneffective
Moderate - Oral corticosteroids potentially with antibiotics ,gradually tapered off, addition of infliximab if needed
Severe - IV corticosteroids with antibiotics, with infliximab and surgery is required

Question 63

How do you take a GI history?

Answer 63

Key symptoms to consider include:
Upper GIT: jaundice, apthous ulceration, vomiting, haematemesis, acid reflux, dyshagia, odynophagia

Lower GIT symptoms: pain, abdomeinal distention, contisptaion, diarrhoea (with blood), malaena, bleeding rectum fresh blood

Symstemic: anorexia, weight fluctuation, nausea, fatigue, fever, confusion

Important risk factors: pre-existing GIT disease, family history of GIT disease, alcohol, smoking, recreational drugs, diet

Question 64

How do you conduct an abdominal examination?

Answer 64

Patient lying flat on the beg, arms to their side and legs uncrossed.
Exposed from waist up (may keep bra on)
Inspect for scars, distention, ceput medisae, stretch marks, hernias, bruising in the flanks
Not the presence and features of any stomas
Ask if the patient is any pain
Light palpate all nine quadrants of the abdomen
Deep palpate all nine quadrants of the abdomen
Notice any (rebound) tenderness, guarding, masses
Palpate the liver from the right illiac fossa upwards, use a sweeping motion pushing inwards and upwards whilst the patient takes a deep breath in and removing when they take a deep breath out
If liver edge is identified, palpate the degree of extension below the costal margin, smoothness of the edge
My try to palpitate the gall bladder at midclavicular right costal margin moves with respiration _not normally felt
Palpate the spleen starting the the right illiac fossa and heading towards the spleen
Ballot the kidneys using force from above and below
May also palpate the bladder and the abdominal aorta
Percuss the liver, spleen and bladder
Assess shifting dullness (ascites)
Listen for bowel sounds

Question 65

What are crohns flares ups and what can cause them?

Answer 65

Repeated symptomatic episode of diarrhoea and othe rsymptosm after previously experiencing remission

Can be caused by: missing a dose of medication, NSAIDs, antibiotics, smoking, infections.
Worsened by: stress, certain foods .

Question 66

How is IBS diagnosed?

Answer 66

Clinical diagnosis - syndrome of symptoms
Unable to diagnose with something else
Is no positive test for IBS
Typically bowel shows no structural damage or signs of inflammation on endoscopy.

Question 67

How do you test for faecal calprotectin?

Answer 67

4 weeks before: stop taking NSAIDs and antibiotics, avoid collecting water and urine into the test container.
Detected by immunoassay

Question 68

What is the NHS e-referall system?

Answer 68

Online system
Allows GPs and other health care professionals to request that their patients receive an appointment from a different speciality
Uase by patients to choose their first hospital or clinic appointment with a specialist, bookings can be made online, using a telephone or directly in the GP surgery at the time or referral (urgent referall).
Creates online centralise patient records

Maximum waiting times are:
18 weeks for non-urgent appointments
2 weeks for suspected cancer
48 hours for an urgent referall

Question 69

What is the role of the NHS e-referal system in IBD diagnosis?

Answer 69

GP Urgent Referall to gastronenterologist and later referal to dietitian
Online system allows good communication between different members of the team, providing synchronous and continuous care for the patient

Question 70

What is Rosies explanation for the pathophysiology of IBD?

Answer 70

Normal barrier function is impaired by genetic and environmental risk factors - noticeable disruption of tight junction
Leads to increased permeability of the epithelium to commensals and pathogens including microbial products
Macrophages and dendtiric cell recognition of pathogen resulting in T cell activation
Leads to production of interleukins, pro-inflammatory cytokines such as TNF-alpha. Activation of intra-epithelial lymphocytes to kill epithelial cells
If acute inflammation is not resolves, progresses to chronic inflammation resulting in tissue destruction, stenosis and even cancer

Question 71

What treatment is used for iron deficiency anaemia in IBD?

Answer 71

May be prescribed ferrous sulphate tablets everyday and for three months after deficiency has been corrected : synthetic iron supplements
Iron is absorbed by FMT1 across the duodenal brush border into epithelial cells.
Is then oxidised to iron Fe3+ and sequester by transferrin for transport in the blood.

Oral use is only suitable if the patient deficiency is due to dietary factors rather than malbasoprtion, if needed should be given as IV

Question 72

What are some common side effects of immunsuppresants?

Answer 72

Vulnerable to opportunisitic infections, which are then harder to treat
Hair loss
Mouth sores
Osteoporosis
Acne
Fatigue
High blood pressure

Question 73

What is the role of an IBD specialist nurse?

Answer 73

Provide expert support and advice for people living with Crohn’s and Colitis under the care of specialist IBD services. Encourage self-management where possible
Involved in support at diagnosis and ongoing, patient education, counselling and monitoring medication, co-ordinating and referal to other health professionals as required. Provide a link between hospital and community services.

Question 74

What is the role of the gastroenterologist?

Answer 74

A doctor who treats digestive disorders including the alimentary canal and the billary organs, including pancrease, liver and bowel
Typically work in hospitals and outpatient clinics.

Role in diagnostic tests and treatment management

Are not surgeons – work alongside gastrointestinal surgeons

Question 75

What is the role of a dietitian?

Answer 75

The only qualified health care professional who can assess, diagnose and treat nutritional related health problems at the individual and public health level.
Typically identify nutritional needs and work alongside the patient to find plausible ways of meeting their nutritional goals.
Translate guidance into practical advice
Normally become involved with patients who have complex health needs or have a concerning BMI with health complications

Question 76

How does IBD demonstrate health inequalities in minority ethnic groups?

Answer 76

Cultural foods - may be less understood by dietitian and harder to incorporate into diet plan, many spciy foods that may be preferred are thought to trigger inflammation

Stimga - less likely to go the GP with a personal issue such as diarrhoea, may be embarrassed, view as a dirty problems that shouldn’t be shared outside of the household

Assumptions based on race - diagnosed with lactose intolerance incorrectly - problems continue to worsen as effective treatment is not given

LIC - lack of diagnostic tools, often thought to be a result of an infection such as cholera, poor sanitation means more social stigma and embarrassment for the indivdual

Question 77

What are the gendered social norms on GIT problems?

Answer 77

1. Females less likley to seek help, embarrased to share an intimate diagnosis with a male doctor. Flatulence and discussions around bowel movements are not very lady like
2. Males may find it harder to manage symptoms when out of home, male toilers often only one to two cubiles can be more obvious when suffering from bowel movements
3. Socially comical for a man to have diahorrea or to go to the bathroom when he needs to, females more secretive about this behaviour

Question 78

What is meant by biographical disruption? Link to crohns disease

Answer 78

A significant, sudden change that alters an individuals life that changes its plans and directions
Crohns diagnosis - ability to work, go to education, ability to travel, ability to complete activities

Question 79

What is the stage of coping with a chronic illness?

Answer 79

Disavowl - lack of control and noramlity
False normality - partial control but not long standing
The new normal - acceptance is achieved, less vulnerable to stress
Disruption - exposure to stressful situation illness or not

Question 80

What are the risk factors for Crohn’s disease?

Answer 80

Smoking - 1.76x, is immunosuppressive, decreased neutrophil activity and reducing chemotaxic and cytokine signalling
Family history - children and siblings 17-35x more likely
Drugs - NSAIDs, oral contraceptive
Diet - effects gut microbiome, high fat and low plant fibre diet has the greatest risk
Age - before 30yrs
Ethnicity - white, dietary and genetic links NOD2 and IL23R mutations

Question 81

What are the products of lactose fermentation by gut bacteria?

Answer 81

H2 CO2 and CH4
Alongside short chain fatty acid production including
Propionate, acetate and butyrate

Question 82

What is the rectalanal inhibtory reflex?

Answer 82

rectum distendts
Inhibitory signlas in teh anus - causing to relxa and distend to accommodate the movement of faeces

Question 83

How are antibodies used to test for coeliac disease

Answer 83

IgA tTG antibodies are tested for
Gliadin is a part of gluten broken down into peptides, these are modified by transglutaminase (TG)
TG associated with peptides triggers an immune response