GI Flashcards
(108 cards)
1
Q
Features of constipation
A
reduced stool frequency and harder stools
2
Q
What is faecal impaction?
A
Faecal impaction refers to when chronic constipation leads to a large build-up of hard stools in the rectum and bowel. The stool blocks the rectum, and the child stops being able to open their bowels. The only stools that can get past the impaction are very loose and tend to be smelly. It can lead to overflow soiling with smelly loose stools.
3
Q
Idiopathic/ Functional Constipation causes
A
Idiopathic constipation, or functional constipation, is when there is no underlying physical cause other than lifestyle and environmental factors. Contributing lifestyle and environmental factors include:
Reduced fluid intake
Reduced fibre intake
Reduced physical activity
Psychosocial issues (e.g., toilet training problems, stress or abuse)
4
Q
Secondary causes of constipation
A
Hirschsprung’s disease
Cystic fibrosis (particularly meconium ileus)
Hypothyroidism
Medications (e.g., antihistamines or opiates)
5
Q
Presenting features of constipation include:
A
Reduce frequency of bowel movements (e.g., less than three times per week)
Hard or large stools that are difficult to pass
Rabbit-dropping stools (small round stools)
Straining
Painful passage of stools
Overflow soiling (incontinence of particularly smelly loose stools)
Rectal bleeding associated with hard stools
Abdominal pain
Holding an abnormal posture, referred to as retentive posturing
Hard stools may be palpable on abdominal examination
6
Q
Red flags for constipation that may indicate a serious underlying condition and require prompt referral and investigations include:
A
Not passing meconium within 48 hours of birth (cystic fibrosis or Hirschsprung’s disease)
Neurological signs or symptoms, particularly in the lower limbs (cerebral palsy or spinal cord lesion)
Vomiting (intestinal obstruction or Hirschsprung’s disease)
Ribbon stool (anal stenosis)
Abnormal anus (infection, stenosis, inflammatory bowel disease or sexual abuse)
Abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis)
Failure to thrive (coeliac disease, hypothyroidism, cystic fibrosis or safeguarding issues)
Acute severe abdominal pain and bloating (obstruction or intussusception)
7
Q
Complications of constipations
A
Pain
Anal fissures
Haemorrhoids
Overflow and soiling
Psychosocial morbidity
8
Q
Behavioural and lifestyle interventions for constipation
A
Sufficient fluid intake
Sufficient fibre intake
Sufficient physical activity
Regular attempts to open the bowel (e.g., after each meal)
Bowel movement chart
Encouragement systems (e.g., star charts)
9
Q
Initial treatment for constipation in children involves:
A
Macrogol laxatives (e.g., Movicol paediatric) first-line
Stimulate laxatives (e.g., Senna) second-line
10
Q
How do macrogol laxatives work?
A
Paediatric macrogol laxatives contain polyethylene glycol (macrogol) and electrolytes. They are osmotic laxatives, and they work by drawing water into the stool, making it softer and easier to pass. The dose is escalated as required until regular soft stools are achieved. Lactulose is a common alternative osmotic laxative.
11
Q
Tx for faecal impaction
A
For faecal impaction, the dose (of macrogol) is escalated every few days, up to a maximum of 8-12 sachets daily, depending on their age (specific regimes are found in the BNF).
12
Q
What is a diverticulum?
A
A diverticulum (plural diverticula) is a pouch or pocket in the bowel wall, usually ranging in size from 0.5 – 1cm.
13
Q
What is diverticular disease?
A
Diverticular disease is a common surgical problem. It consists of the herniation of colonic mucosa through the muscular wall of the colon. The usual site is between the taenia coli where vessels pierce the muscle to supply the mucosa. For this reason, the rectum, which lacks taenia, is often spared.
14
Q
What is diverticulosis?
A
Diverticulosis refers to the presence of diverticula, without inflammation or infection. Diverticulosis may be referred to as diverticular disease when patients experience symptoms.
15
Q
What is diverticulisis?
A
Diverticulitis refers to inflammation and infection of diverticula.
16
Q
Symptoms of diverticular disease?
A
Altered bowel habit
rectal bleeding
Abdominal pain
17
Q
Pathophysiology of diverticular disease?
A
The wall of the large intestine contains a layer of muscle called the circular muscle. The points where this muscle layer is penetrated by blood vessels are areas of weakness. Increased pressure inside the lumen over time, can cause a gap to form in these areas of the circular muscle. These gaps allow the mucosa to herniate through the muscle layer and pouches to form (diverticula).
18
Q
Why do diverticula not form in the rectum?
A
Diverticula do not form in the rectum, because it has an outer longitudinal muscle layer that completely surrounds the diameter of the rectum, adding extra support. In the rest of the colon, there are three longitudinal muscles that run along the colon, forming strips or ribbons called teniae coli. The teniae coli do not surround the entire diameter of the colon, and the areas that are not covered by teniae coli are vulnerable to the development of diverticula.
19
Q
Where is diverticulosis found?
A
it can affect the entire large intestine in some patients. Small bowel diverticula are also possible but much less common.
20
Q
Which area of the bowel is most commonly affected by diverticulosis?
A
Signmoid colon
21
Q
Risk factors for diverticulosis
A
Diverticulosis is very common with increased age. Low fibre diets, obesity and the use of NSAIDs are risk factors. The use of NSAIDs increases the risk of diverticular haemorrhage.
22
Q
Dx of diverticulosis
A
It is often diagnosed incidentally on colonoscopy or CT scans. Treatment is not necessary where the patient is asymptomatic.
23
Q
Advice for patients who have diverticulosis
A
High fibre diet + weight loss
24
Q
Sx of diverticulosis
A
lower left abdominal pain, constipation or rectal bleeding
25
Management of diverticulosis
Management is with increased fibre in the diet and bulk-forming laxatives (e.g., ispaghula husk). Stimulant laxatives (e.g., Senna) should be avoided. Surgery to remove the affected area may be required where there are significant symptoms.
26
Presentation of acute diverticulitis
Pain and tenderness in the left iliac fossa / lower left abdomen
Fever
Diarrhoea
Nausea and vomiting
Rectal bleeding
Palpable abdominal mass (if an abscess has formed)
Raised inflammatory markers (e.g., CRP) and white blood cells
27
Management of uncomplicated acute diverticulitis
The NICE clinical knowledge summaries (updated January 2021) suggest management of uncomplicated diverticulitis in primary care with:
Oral co-amoxiclav (at least 5 days)
Analgesia (avoiding NSAIDs and opiates, if possible)
Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)
Follow-up within 2 days to review symptoms
28
Acute diverticulitis: Patients with severe pain or complications require admission to hospital. Hospital treatment involves management as with any patient with an acute abdomen or sepsis, including:
Nil by mouth or clear fluids only
IV antibiotics
IV fluids
Analgesia
Urgent investigations (e.g., CT scan)
Urgent surgery may be required for complications
29
Complications of acute diverticulitis
Perforation
Peritonitis
Peridiverticular abscess
Large haemorrhage requiring blood transfusions
Fistula (e.g., between the colon and the bladder or vagina)
Ileus / obstruction
30
What is GORD?
Gastro-oesophageal reflux disease (GORD) is where acid from the stomach flows through the lower oesophageal sphincter and into the oesophagus, where it irritates the lining and causes symptoms.
31
What is the difference in the lining of the oesophagus and the stomach?
The oesophagus has a squamous epithelial lining that makes it more sensitive to the effects of stomach acid. The stomach has a columnar epithelial lining that is more protected against stomach acid.
32
Certain factors can exacerbate or worsen the symptoms of GORD:
Greasy and spicy foods
Coffee and tea
Alcohol
Non-steroidal anti-inflammatory drugs
Stress
Smoking
Obesity
Hiatus hernia
33
Presentation of GORD
Dyspepsia is a non-specific term used to describe indigestion. It covers the symptoms of GORD:
Heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice
34
Red flags for GORD
Dysphagia (difficulty swallowing) at any age gets an immediate two week wait referral
Aged over 55 (this is generally the cut-off for urgent versus routine referrals)
Weight loss
Upper abdominal pain
Reflux
Treatment-resistant dyspepsia
Nausea and vomiting
Upper abdominal mass on palpation
Low haemoglobin (anaemia)
Raised platelet count
35
What happens to those suspected of cancer with GORD presentation?
Patients with symptoms suspicious of cancer get a two week wait referral for further investigation. It is possible to refer from primary care for an urgent direct-access endoscopy. The NICE guidelines on suspected cancer (2021) have criteria for when to refer urgently or routinely.
36
What is an OGD?
An oesophago-gastro-duodenoscopy (OGD) involves inserting a camera through the mouth down to the oesophagus, stomach and duodenum. It can be used to assess for:
Gastritis
Peptic ulcers
Upper gastrointestinal bleeding
Oesophageal varices (in liver cirrhosis)
Barretts oesophagus
Oesophageal stricture
Malignancy of the oesophagus or stomach
37
Sign of upper GI bleeding
Melaena or coffee ground vomiting
38
What is a hiatus hernia?
A hiatus hernia refers to the herniation of the stomach up through the diaphragm. The diaphragm opening should be at the lower oesophageal sphincter level and fixed in place. A narrow opening helps to maintain the sphincter and stops acid and stomach contents from refluxing into the oesophagus. When the opening of the diaphragm is wider, the stomach can enter through the diaphragm, and the contents of the stomach can reflux into the oesophagus.
39
What are the 4 types of hiatus hernia?
Type 1: Sliding
Type 2: Rolling
Type 3: Combination of sliding and rolling
Type 4: Large opening with additional abdominal organs entering the thorax
40
What is a sliding hiatus hernia?
A sliding hiatus hernia is where the stomach slides up through the diaphragm, with the gastro-oesophageal junction passing up into the thorax.
41
What is a rolling hiatus hernia?
A rolling hiatus hernia is where a separate portion of the stomach (i.e., the fundus), folds around and enters through the diaphragm opening, alongside the oesophagus.
42
What is Type 4 hiatus hernia?
Type 4 hiatus hernia refers to a large hernia that allows other intra-abdominal organs to pass through the diaphragm opening (e.g., bowel, pancreas or omentum).
43
Hiatus hernias can be intermittent, meaning they may not be seen on investigations. Hiatus hernias may be seen on a:
Chest x-ray
CT scan
Endoscopy
Barium swallow test
44
Management of gastro-oesophageal reflux disease can be split into:
Lifestyle changes
Reviewing medications (e.g., stop NSAIDs)
Antacids (e.g., Gaviscon, Pepto-Bismol and Rennie) – short term only
Proton pump inhibitors (e.g., omeprazole and lansoprazole)
Histamine H2-receptor antagonists (e.g., famotidine)
Surgery
45
GORD Lifestyle changes include:
Reduce tea, coffee and alcohol
Weight loss
Avoid smoking
Smaller, lighter meals
Avoid heavy meals before bedtime
Stay upright after meals rather than lying flat
46
Surgery for GORD
Surgery for reflux is called laparoscopic fundoplication. This involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.
47
What is H.pylori?
Helicobacter pylori (H. pylori) is a gram-negative aerobic bacteria that can live in the stomach. It causes damage to the epithelial lining, resulting in gastritis, ulcers and an increased risk of stomach cancer. It avoids the acidic environment by forcing its way into the gastric mucosa, using flagella to propel itself. It creates gaps in the mucosa, exposing the epithelial cells underneath to damage from stomach acid.
H. pylori produces ammonium hydroxide, which neutralises the acid surrounding the bacteria. It also produces several toxins. The ammonia and toxins lead to gastric mucosal damage.
48
Who is H.pylori testing offered to?
We offer a test for H. pylori to anyone with dyspepsia. They need 2 weeks without using a PPI before testing for H. pylori for an accurate result.
49
Ix for H.pylori
Stool antigen test
Urea breath test using radiolabelled carbon 13
H. pylori antibody test (blood)
Rapid urease test performed during endoscopy (also known as the CLO test)
50
What is a rapid urease test?
A rapid urease test involves taking a small biopsy of the stomach mucosa. This is added to a liquid medium containing urea. H. pylori produce urease enzymes that convert urea to ammonia. Ammonia makes the solution more alkaline. A pH indicator (e.g., phenol red) changes colour if the pH rises, giving a positive result.
51
Tx for H.pylori infection
The H. pylori eradication regime involves triple therapy with a proton pump inhibitor (e.g., omeprazole) plus two antibiotics (e.g., amoxicillin and clarithromycin) for 7 days. Routine re-testing is not necessary after treatment.
52
What is Barrett's Oesophagus ?
Barrett’s oesophagus refers to when the lower oesophageal epithelium changes from squamous to columnar epithelium. This process is called metaplasia. It is caused by chronic acid reflux into the oesophagus. Patients may notice improved reflux symptoms after they develop Barrett’s oesophagus.
Barrett’s oesophagus is a premalignant condition and a significant risk factor for developing oesophageal adenocarcinoma (cancer of the epithelial cells). There can be a stepwise progression from no dysplasia to low-grade dysplasia, high-grade dysphasia, and adenocarcinoma.
53
Tx of Barrett's Oesophagus
Endoscopic monitoring for progression to adenocarcinoma
Proton pump inhibitors
Endoscopic ablation (e.g., radiofrequency ablation)
54
What is endoscopic ablation?
Ablation can be used to destroy abnormal columnar epithelial cells, which are then replaced with normal squamous epithelial cells. Ablation has a role in treating low and high-grade dysplasia to reduce cancer risk.
55
What is Zollinger-Ellison Syndrome?
Zollinger-Ellison syndrome is a rare condition where a duodenal or pancreatic tumour secretes excessive quantities of gastrin. Gastrin is a hormone that stimulates acid secretion in the stomach. Therefore, there is excess production of stomach acid, resulting in severe dyspepsia, diarrhoea and peptic ulcers.
Gastrin-secreting tumours (gastrinomas) may be associated with multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant genetic condition, which can also cause hormone-secreting tumours of the parathyroid and pituitary glands.
56
What is haemorrhoids ?
Haemorrhoids are enlarged anal vascular cushions. It is not clear why they become enlarged and swollen, but they are often associated with constipation and straining. They are also more common with pregnancy, obesity, increased age and increased intra-abdominal pressure (e.g., weightlifting or chronic coughing).
57
When do haemorrhoids commonly occur?
They often occur in pregnancy, most likely due to constipation, pressure from the baby in the pelvis and the effects of hormones that relax the connective tissues.
58
Risk factors for haemorrhoids
Constipation: this will predispose the patient to increase time straining on the toilet
Increased age
Increased abdominal pressure, such as in pregnancy and labour
Diarrhoea
High BMI
59
What are anal cushions?
The anal cushions are specialised submucosal tissue that contain connections between the arteries and veins, making them very vascular. They are supported by smooth muscle and connective tissue. They help to control anal continence, along with the internal and external sphincters. The blood supply is from the rectal arteries.
The location of pathology at the anus is described as a clock face, as though the patient was in the lithotomy position (on their back with their legs raised). 12 o’clock is towards the genitals and 6 o’clock is towards the back. The anal cushions are usually located at 3, 7 and 11 o’clock.
60
What does the classification of haemorrhoids depend on?
The classification of haemorrhoids depends on their size and whether they prolapse from the anus. Haemorrhoids are classified using Goligher’s classification
61
What are the different classifciations of haemorrhoids?
1st degree: no prolapse ; anal cushions bleed but remain in the rectum
2nd degree: prolapse when straining and return on relaxing (spontaneously reduces)
3rd degree: prolapse when straining, do not return on relaxing, but can be pushed back (requires manual reduction)
4th degree: prolapsed permanently
62
Symptoms of haemorrhoids
Haemorrhoids may be asymptomatic. They are often associated with constipation and straining.
A common presentation is with painless, bright red bleeding, typically on the toilet tissue or seen after opening the bowels. The blood is not mixed with the stool (this should make you think of an alternative diagnosis).
Other symptoms include:
Sore / itchy anus
Feeling a lump around or inside the anus
63
Examination findings for haemorrhoids
External (prolapsed) haemorrhoids are visible on inspection as swellings covered in mucosa
Internal haemorrhoids may be felt on a PR exam (although this is generally difficult or not possible)
They may appear (prolapse) if the patient is asked to “bear down” during inspection
64
What is proctoscopy for haemorrhoids?
Proctoscopy is required for proper visualisation and inspection. This involves inserting a hollow tube (proctoscope) into the anal cavity to visualise the mucosa.
65
Differentials for haemorrhoids
Consider the differential diagnoses in patients presenting with symptoms such as rectal bleeding:
Anal fissures
Diverticulosis
Inflammatory bowel disease
Colorectal cancer
66
Topical treatment for haemorrhoids
Topical treatments can be given for symptomatic relief and to help reduce swelling, for example:
Anusol (contains chemicals to shrink the haemorrhoids – “astringents”)
Anusol HC (also contains hydrocortisone – only used short term)
Germoloids cream (contains lidocaine – a local anaesthetic)
Proctosedyl ointment (contains cinchocaine and hydrocortisone – short term only)
67
Prevention + tx for constipation with haemorrhoids
Increasing the amount of fibre in the diet
Maintaining a good fluid intake
Using laxatives where required
Consciously avoiding straining when opening their bowels
68
Non-surgical Tx for haemorrhoids
Rubber band ligation (fitting a tight rubber band around the base of the haemorrhoid to cut off the blood supply)
Injection sclerotherapy (injection of phenol oil into the haemorrhoid to cause sclerosis and atrophy)
Infra-red coagulation (infra-red light is applied to damage the blood supply)
Bipolar diathermy (electrical current applied directly to the haemorrhoid to destroy it)
69
Surgical options for haemorrhoids
Haemorrhoidal artery ligation involves using a proctoscope to identify the blood vessel that supplies the haemorrhoids and suturing it to cut off the blood supply.
Haemorrhoidectomy involves excising the haemorrhoid. Removing the anal cushions may result in faecal incontinence.
Stapled haemorrhoidectomy involves using a special device that excises a ring of haemorrhoid tissue at the same time as adding a circle of staples in the anal canal. The staples remain in place long-term.
70
What are thrombosed haemorrhoids?
Thrombosed haemorrhoids are caused by strangulation at the base of the haemorrhoid, resulting in thrombosis (a clot) in the haemorrhoid. This can be very painful.
71
Presentation of thrombosed haemorrhoids
Thrombosed haemorrhoids appear as purplish, very tender, swollen lumps around the anus. A PR examination is unlikely to be possible due to the pain.
72
Management of thrombossed haemorrhoids
They will resolve with time, although this can take several weeks.
The NICE Clinical Knowledge Summaries (2016) suggests considering admission if the patient present within 72 hours with extremely painful thrombosed haemorrhoids. They may benefit from surgical management.
73
What is IBS?
Irritable bowel syndrome (IBS) is caused by a disturbance of the gut-brain interaction, resulting in troublesome abdominal and intestinal symptoms. Symptoms can significantly impact the patient’s life.
Irritable bowel syndrome is a functional disorder. This means there is no identifiable bowel disease underlying the symptoms, and the symptoms result from the abnormal functioning of an otherwise normal bowel.
74
Epidemiology of IBS?
It occurs in up to 20% of the population. It affects women more than men and is more common in younger adults.
75
Causes of IBS?
The exact cause of IBS is unknown, and it is grouped with other functional disorders (e.g. fibromyalgia, functional dyspepsia), which do not have a measurable pathological hallmark or biomarker. However, advances in research have uncovered several proposed contributing mechanisms, which include:
Disordered gut-brain axis function, which links bowel symptoms to stress hormones and psychosocial factors
Visceral hypersensitivity, whereby there is an exaggerated response of the bowel to certain stimuli (e.g. food)
Abnormal gut motility, which can either lead to decreased or increased colonic transit time (causing constipation or diarrhoea, respectively)
Peripheral bowel factors include alterations in gut microbiota (contributing to post-gastroenteritis IBS) and immune-mediated processes
76
Risk factors for IBS
Age: typically occurs in younger people and is rare to diagnose >50 years old
Gender: more common in females
Mental health history: those with anxiety, depression, or a history of childhood abuse have a higher risk of developing IBS
Recent gastroenteritis: can lead to post-infectious IBS, impacted by the duration/type of infection and whether antibiotics were used
Family history: genetic predisposition to developing IBS
77
Red flag Sx for IBS
IBS should not present with red flags symptoms, and any of these should prompt further assessment and investigation:
Rectal bleeding
Weight loss (unexplained)
Age >50 years
Family history of bowel/ovarian cancer, inflammatory bowel disease, coeliac disease
Abdominal/rectal mass
Significant/focal tenderness
Iron deficiency anaemia
Stigmata of bowel cancer or inflammatory bowel disease (e.g. cachexia, clubbing, uveitis)
78
Key features of IBS
I – Intestinal discomfort (abdominal pain relating to the bowels)
B – Bowel habit abnormalities
S – Stool abnormalities (watery, loose, hard or associated with mucus)
79
Common symptoms of IBS
Abdominal pain
Diarrhoea
Constipation
Fluctuating bowel habit
Bloating
Worse after eating
Improved by opening bowels
Passing mucus
80
Triggers for worsening IBS symptoms
Anxiety
Depression
Stress
Sleep disturbance
Illness
Medications
Certain foods
Caffeine
Alcohol
81
Differential Dx for IBS
Bowel cancer
Inflammatory bowel disease
Coeliac disease
Ovarian cancer (often presents with vague symptoms, particularly bloating in women over 50 years)
Pancreatic cancer
82
Ix for IBS
Full blood count for anaemia
Inflammatory markers (e.g., ESR and CRP)
Coeliac serology (e.g., anti-TTG antibodies)
Faecal calprotectin for inflammatory bowel disease
CA125 for ovarian cancer
83
Dx of IBS
The NICE clinical knowledge summaries (updated 2022) suggest before a diagnosis, differentials need to be excluded, and the patient should have at least 6 months of abdominal pain or discomfort with at least one of:
Pain or discomfort relieved by opening the bowels
Bowel habit abnormalities (more or less frequent)
Stool abnormalities (e.g., watery, loose or hard)
For a diagnosis, patients also require at least two of:
Straining, an urgent need to open bowels or incomplete emptying
Bloating
Worse after eating
Passing mucus If alternative diagnoses are excluded and no red flag features are present, a positive diagnosis of IBS can be made in primary care
84
Lifestyle advice for IBS
Drinking enough fluids
Regular small meals
Adjusting fibre intake according to symptoms (more fibre if predominantly constipated, less with diarrhoea/bloating)
Limit caffeine, alcohol and fatty foods
Low FODMAP diet, guided by a dietician
Probiotic supplements may be considered over-the-counter (discontinuing after 12 weeks if there is no benefit)
Reduce stress where possible
Regular exercise
85
First line medications for IBS (depend of symptoms)
Loperamide for diarrhoea
Bulk-forming laxatives (e.g., ispaghula husk) for constipation (lactulose can cause bloating and is avoided)
Antispasmodics for cramps (e.g., mebeverine, alverine, hyoscine butylbromide or peppermint oil)
86
Other medications that can be used for IBS
There is only weak evidence for the benefit of using antispasmodic medications, and they may cause side effects.
Linaclotide is a specialist secretory drug for constipation in IBS when first-line laxatives are inadequate.
Other options include where symptoms remain uncontrolled:
Low-dose tricyclic antidepressants (e.g., amitriptyline)
SSRI antidepressants
Cognitive behavioural therapy (CBT)
Specialist referral for further management
87
What criteria is used to diagnose IBS in secondary care ?
ROME-IV criteria
88
What is the ROME-IV criteria?
This consists of recurrent abdominal pain ≥1 day/week in the last 3 months (on average) with ≥2 of the following:
Symptoms related to defecation
Associated with change in stool frequency
Associated with change in stool form
The ROME-IV criteria can also categorise IBS into different sub-types.
89
IBS subtypes
Using the above criteria and the Bristol stool chart, IBS can be sub-classified into:
IBS-D (IBS with diarrhoea): >25% type 6-7 stools and <25% type 1-2 stools
IBS-C (IBS with constipation): >25% type 1-2 stools and <25% type 6-7 stools
IBS-M (IBS with mixed bowel habits): >25% type 1-2 stools and type 6-7 stools
IBS-U (unclassified IBS): meets diagnostic criteria, but bowel habits not accurately classified
90
91
Epidemiology of Obesity?
According to World Health Organisation (WHO), obesity is a global epidemic, with 4 million people dying annually due to the disease. In the UK, 1 in 4 adults and 1 in 5 children are obese
92
Risk factors for Obesity
he main risk factors for obesity include poor diet and lack of physical activity.
Other risk factors include:
Underlying medical conditions: Cushing’s syndrome, polycystic ovarian syndrome (PCOS), hypothyroidism and growth hormone deficiency
Medications: antidepressants (tricyclics, monoamine oxidase inhibitors, mirtazapine, atypical antipsychotics) and corticosteroids
Socio-economic status: access to healthy food, education about healthy diet
Mental health: depression, eating disorders (e.g. binge eating disorder, emotional eating)
Genetics: rare genetic conditions, such as Prader-Willi syndrome and Bardet-Biedl syndrome, can result in obesity
Although genetics has been shown to play a role in regulating body weight, behavioural and environmental factors are deemed the main contributors to obesity.
93
What is Metabolic Syndrome?
Metabolic syndrome is a term used to describe a group of risk factors including hypertension, hyperglycaemia, excess fat around the waist, and hypercholesterolemia. It increases the likelihood of developing diabetes, stroke, and heart disease.
94
BMI classifcation
Healthy weight: BMI of 18.5-24.9 kg/m2
Overweight: BMI of 25-29.9 kg/m2
Obesity class I: BMI of 30-34.9 kg/m2
Obesity class II: BMI of 35-39.9 kg/m2
Obesity class III: BMI of 40 kg/m2 or greater
95
Ix for Obesity
Fasting blood glucose: diabetes
Lipid profile: hyperlipidaemia
Liver function tests (LFTs): non-alcoholic fatty liver disease
Thyroid-stimulating hormone (TSH): hypothyroidism
Urea and electrolytes (U&Es): chronic kidney disease
Specific tests such as dexamethasone suppression test for Cushing’s syndrome, TSH for hypothyroidism, and ultrasound for polycystic ovarian syndrome can be requested if an underlying disease process is suspected
96
Management of Obesity
Obesity is managed by weight loss, with a target of a 5-10% reduction in body weight.
97
98
Lifestyle changes for managing obesity
encouraging regular exercise, healthy eating, alcohol recommendations and smoking cessation and therapy focused on behavioural changes
99
Medications for obesity management + how do they work
Orlistat - orally -pancreatic lipase inhibitor: prevents the absorption of dietary fat.
Liraglutide- Subcut Injection OD - GLP1 analogue - delays gastric emptying and induces early satiety.
100
SE for Orlistat
flatus with oily spotting and loose stools
101
When should Orlistat be prescribed?
BMI of 28 kg/m^2 or more with associated risk factors, or
BMI of 30 kg/m^2 or more
continued weight loss e.g. 5% at 3 months
orlistat is normally used for < 1 year
102
SE for Liraglutide
N+V, diarrrhoea, pancreatitis (1%) and thyroid(papillary) cancer
103
When should Liraglutide be prescribed?
person has a BMI of at least 35 kg/m²
prediabetic hyperglycaemia (e.g. HbA1c 42 - 47 mmol/mol)
104
Surgical options for obesity management
Bariatric surgery - BMI ≥40 kg/m2 or a BMI between 35-40 kg/m2 with co-morbidities such as type 2 diabetes or hypertension.
The most common types of bariatric surgery include the Roux-en-Y gastric bypass, sleeve gastrectomy, and gastric bypass
105
What is Dumping syndrome ?
Dumping syndrome describes a group of symptoms caused by food rapidly emptying or being ‘dumped’ from the stomach into the small intestines. This results in undigested food within the small intestine that the body finds difficult to absorb. Symptoms include sweating, bloating, abdominal cramps/pain, diarrhoea, and nausea.
106
Complications of Obesity
Obesity is associated with increased mortality and morbidity.
Obesity-related complications include cardiovascular disease (e.g. hypertension, coronary heart disease), dyslipidaemia, diabetes, stroke, obstructive sleep apnoea, and cancer
107
What is Leptin ?
Leptin is thought to play a key role in the regulation of body weight. It is produced by adipose tissue and acts on satiety centres in the hypothalamus and decreases appetite. More adipose tissue (e.g. in obesity) results in high leptin levels.
Leptin stimulates the release of melanocyte-stimulating hormone (MSH) and corticotrophin-releasing hormone (CRH). Low levels of leptin stimulates the release of neuropeptide Y (NPY)
108
What is Ghrelin?
Where as leptin induces satiety, ghrelin stimulates hunger. It is produced mainly by the P/D1 cells lining the fundus of the stomach and epsilon cells of the pancreas. Ghrelin levels increase before meals and decrease after meals
