3. Presentation & Pathophysiology of GI Conditions Flashcards
(67 cards)
1
Q
Layers of the GIT (4)
A
- Mucosal layer
- Submucosal layer
- Muscularis layer
- Serosa layer
2
Q
Upper GI Tract – Oral cavity to duodenum: Common disorders
A
- Gastro-oesophageal reflux disease (GORD)
- Peptic ulcer disease (PUD)
- Functional dyspepsia
- These conditions can often have overlapping symptoms
- An individual may also have more than one of these conditions
3
Q
Peristalsis & LOS relaxation:
A
- Upper sphincter relaxes when larynx is lifted
- Peristalsis pushes food down
+ Circular fibres behind bolus
+ Longitudinal fibres in front of bolus shorten the distance of travel - Travel time is 4-8 seconds for solids & 1 sec for liquids
- Lower sphincter relaxes as food approaches
4
Q
GORD: Pathophysiology
A
- Gastro-oesophageal reflux is the movement of gastric contents into the oesophagus
- Reflux occurs in normal physiological situation:
+ LOS relaxes intermittently during the day to let air out of stomach = transient LOS relaxation - Transient LOS relaxation, however, can be excessive:
+ Becomes pathological when to much gastric juice also refluxes into oesophagus causing symptoms/disease
+ Gastric contents contain acid, erosive to oesophagus
5
Q
Other contributing mechanisms of GORD (3)
A
- Hypotensive LOS i.e. not contracting tight enough
- Caffeine, alcohol, chocolate, fats
- Certain medications e.g. beta blockers, nitrates, calcium channel blockers - Hiatus hernia
- Note: Not all people with hiatus hernia have reflux
- Relevant, but not main part of the pathophysiology - Impaired oesophageal peristalsis
- Reduced clearance
6
Q
Hiatus hernia
A
- The hiatus is an opening in the diaphragm, where the oesophagus passes through to join the stomach
- The diaphragm acts as additional support, like a sphincter, constricting around the GO junction
- A hernia is when part of an organ protrudes through an opening in the muscle/tissue that is meant to hold it in place
7
Q
Symptoms of GORD (4)
A
- Heartburn/chest discomfort
- Burning sensation or discomfort over the chest - Regurgitation
- Food or liquid coming back up into the mouth - Sour or bitter taste in mouth
- May worse after eating or lying down (e.g. bed time)
8
Q
Complications of GORD (4)
A
- Reflux oesophagitis
- Peptic stricture
- Barrett’s oesophagus
- Cancer – oesophageal adenocarcinoma
9
Q
- Reflux oesophagitis
A
- Damage to oesophageal mucosa by reflux leading to inflammation, ulceration & bleeding
- Odynophagia (painful swallowing)
- Haematemesis (blood in vomit)
- Dysphagia (difficulty swallowing or food sticking)
10
Q
- Peptic Stricture
A
- Prolonged inflammation of oesophageal mucosa by reflux can lead to fibrosis and scarring
- Dysphagia (difficulty swallowing or food sticking)
11
Q
- Barrett’s oesophagitis & its presentation
A
- Damage to oesophageal epithelium by chronic acid exposure from GORD can lead to Barrett’s oesophagus
- Oesophageal epithelium (squamous epithelium) transforms to become like gastric epithelium (columnar epithelium with goblet cells)
+ Known as intestinal metaplasia - Precursor to oesophageal adenocarcinoma i.e. increased risk
How does Barrett’s present?
May not be associated with specific symptoms
High risk of suspicion in:
- Male, over 50
- Increased BMI
- Smoker
- Chronic GORD, especially poorly controlled
12
Q
- Oesophageal cancer in GORD
A
- 2 types: adenocarcinoma (adenoCa), squamous cell carcinoma (SqCC)
- GORD increases risk of oesophageal adenoCa
+ Chronic poorly treated GORD -> Barrett’s -> adenocarcinoma - Smoking, alcohol, certain dietary food increase risk of oesophageal SqCC
- In western countries, oesophageal adenoCa more common
13
Q
Alarm features in GORD (6)
A
- Haematemesis (vomiting blood)
- Odynophagia (painful swallowing)
- Dysphagia (difficulty swallowing)
- Vomiting
- Weight loss
- Not improving with PPI treatment
14
Q
Major functions of the stomach
A
- Food reservoir
- Digests food
- Antrum mixes & grinds up the food
- Controls passage of food into small intestine
- Pylorus regulates size of particles & controls passage of food (chyme) into small intestine
- Gastric acid secretion
- Other secretions
+ Mucus, HCO3-
+ Intrinsic factor, pepsinogen, prostaglandins
15
Q
Gastric motility (4)
A
- Relaxation of fundus (vagovagal reflex)
- Contraction of body & antrum
- Pylorus contracts
- Mixing by retropulsion
- Fundus acts as a food store
- Body & antrum mix food
- Pylorus contracts to limit exit of chyme
16
Q
Gastric acid secretion
A
Gastric acid is secreted by:
- Parietal cells located in body of stomach
- Have proton pumps to secrete HCl
- Secrete ~2 L/day of gastric acid
Gastric acid main role is to sterilise food
- Stomach environment hostile to bacteria except for H. pylori
Gastric acid has limited role in digestion
- Some help in absorption of iron & B12
17
Q
Protection of gastric mucosa from acid (5)
A
Protective factors:
- Mucous layer
- Bicarbonate secretion
- Epithelial barrier regenerates rapidly
- Prostaglandins
- Mucosal blood flow (sweeps hydrogen ions away)
18
Q
Dyspepsia
A
- Dyspepsia describes indigestion – a symptom, not a diagnosis
- Indigestion feels different to different people
- Epigastric discomfort / burning / discomfort
+ May be associated with post-prandial fullness
+ May be associated with early satiety (i.e. full earlier than usual after a meal)
19
Q
Causes of dyspepsia
A
Functional dyspepsia accounts for 75%
The remaining 25%:
- Peptic ulcer disease
- GORD
- Coeliac disease
- Biliary & pancreatic diseases
- Diabetes
- Medications
- & several more
20
Q
Peptic ulcer disease (PUD)
A
- Helicobacter pylori most common
- Other causes:
+ Aspirin
+ NSAIDs
21
Q
H. pylori
A
- Gram-negative bacteria
- Burrows into mucus lining of stomach where it is less acidic
- Up to 85% of people with H. pylori do not have symptoms
- 10-20% lifetime risk of ulcers
- 1-2% lifetime risk of gastric cancer
22
Q
NSAIDs & Aspirin
A
- NSAIDs very common treatment for musculoskeletal conditions
- Aspirin commonly used in people with cardiovascular disease
- Frequent cause of hospital admissions although risk per prescription is low
23
Q
Mechanism of injury with NSAIDs
A
- NSAIDs & aspirin can cause gastric & duodenal ulceration
- This is mainly via systemic (rather than topical) effects
- Main mechanism is inhibition of COX-1 enzyme involved in synthesis of prostaglandin
24
Q
Peptic ulcer disease: Presentation
A
Dyspepsia / epigastric pain
- When hungry, may suggest ulcer is duodenal
- After eating, may suggest ulcer is gastric
Bleeding
- Haematemesis (vomiting blood) or melaena (black stools)
Perforation
- Hole through the GI tract wall
- Severe pain, rigid abdomen
Obstruction (in pylorus or duodenum) from:
- Swelling around ulcer
- Scarring from previous ulcer causing stricture
- Vomiting after eating
25
Functional dyspepsia
For most people with dyspepsia i.e. indigestion, there are no structural or histological abnormalities to explain for their symptoms
Commonest cause of dyspepsia:
- No structural or tissue abnormality
- Functional GI disorders include irritable bowel syndrome & are characterised by negative investigations
Proposed mechanisms
- Impaired stomach emptying / motility
- Hypersensitivity
- Altered gut microbiome
- Psychosocial dysfunction
26
How to treat functional dyspepsia (4)
1. Proton pump inhibitor
2. Prokinetics e.g. domperidone
3. Low dose tricylic anti-depressant
4. Cognitive behavioural therapy/psychotherapy/hypnotherapy
27
Alarm features associated with dyspepsia (6)
1. Overt GI bleeding (haematemesis/vomiting blood or melaena)
2. Vomiting
3. Iron deficiency
4. Age > 50 years & new onset
5. Strong family history of upper GI cancer
6. Weight loss
28
Lower GI Tract – Small intestine & colon: Common disorders
- Infection
- Irritable bowel syndrome (IBS)
- Functional constipation
- Coeliac disease
- Inflammatory bowel disease (IBD):
+ Crohn’s disease & ulcerative colitis
29
Infective gastroenteritis
Acute diarrhoea is almost always caused by infective gastroenteritis
Symptoms include:
1. Diarrhoea, may have bleeding with it
2. Vomiting / nausea
3. Abdominal pain
4. Fever
Typically do not last beyond 2 weeks
- If longer than this, start thinking about causes of chronic diarrhoea
30
Pathogens (3)
Faecal-oral transmission:
1. Bacteria
- Ingestion of toxins produced by bacteria – S. aureus, Bacillus cerus, Clostridium
- Bacteria adheres to mucosa – salmonella, E. coli, Shigella, Campylobacter jejuni, Yersinia, Listeria
2. Viruses
- Rotavirus, adenovirus, norovirus
3. Protozoa
- Giardia lamblia, Cryptosporidium, Entamoeba histolytica
31
Risk factors for infective gastroenteritis (6)
1. Food borne (Eating out, BBQs)
2. Contaminated water sources
3. Travel
4. Daycare / nurseries (rotavirus)
5. Nursing homes (norovirus)
6. Recent antibiotic use (Clostridium difficile)
32
Management of infective gastroenteritis
Symptoms spontaneously resolve & disease is self-limiting
- Exception: beware in immunocompromised individuals
Avoid anti-diarrhoea agents in those with fever or bloody diarrhoea
- May prolong illness
Hydration
33
Helminthiasis & intestinal worms (4)
Refers to parasitic worm infection
Majority are intestinal, but not all
Intestinal worms:
1. Threadworm (pinworm) – most common worm infection in NZ children
2. Tapeworm – sheep farming areas
3. Roundworm – rare in NZ, but one of the most common helminthic infection in the world
4. Hookworm, whipworm – both rare in NZ
34
Threadworm/pinworm (Enterobius vermicularis)
- Most common cause of worm infection in NZ
- School-aged children
Pruritis ani – itchy anus
- Worse at night – female adult worm leaves anus to deposit eggs onto the skin around the anus
- Worm can be seen sometimes with the naked eye on anus or bowel motions
Transmission:
- Infected child scratches anus -> eggs lodge beneath nails -> transfer to clothing & furniture -> uninfected child touches surface, put hand in mouth and swallows eggs
35
Other causes of pruritis ani
Irritation / dermatitis:
- Diarrhoea or straining
- Incontinence
- Scratching
- Over-wiping with toilet paper
- Too much scrubbing with soap & water
- Spicy foods
- Psoriasis
- Other infections e.g. yeast
- Haemorrhoids / anal fissures / skin tags
- Perianal fistula from Crohn’s
- Psychogenic
36
Bowel habit - Normal?
There is no definition for normal bowel frequency, but what is usual for that individual, whether there has been a change, & whether it is causing problems
37
Constipation
Too slow:
- Reduced bowel frequency
- Hard / firm stools
- Straining
38
Chronic constipation
Vast majority of chronic constipation is functional i.e. no organic pathology
In a small number, chronic constipation may be associated with:
- Electrolyte disturbance
- Hormonal – hypothyroidism, diabetes, pregnancy
- Neurological or pelvic muscle disorders
- Obstruction – stricture (diverticular disease related); rectal prolapse
Some medications can also cause constipation e.g. morphine
39
Alarm features with constipation (5)
1. Recent change in bowel habit
2. Blood in bowel motions (except when suggestive of haemorrhoids)
3. Weight loss
4. Iron deficiency
5. Strong family history of colorectal cancer
40
Management of functional constipation (4)
1. Fibre
2. Fluid intake
3. Lifestyle
4. Laxatives – osmotic preferable over stimulant
41
Diarrhoea
Too fast
- Increased bowel frequency
- Loose or watery stools
Remember – acute diarrhoea (< 2 weeks) is almost always infective, but beyond this, start thinking of chronic causes
42
Chronic diarrhoea causes (4)
Long list of causes including:
1. Functional (as part of irritable bowel syndrome)
2. Inflammatory bowel disease
3. Coeliac disease
4. Medications
43
Alarm features with diarrhoea (5)
1. Recent change in bowel habit
2. Blood in bowel motions
3. Weight loss
4. Iron deficiency
5. Strong family history of colorectal cancer
44
Irritable bowel syndrome (IBS)
- Commonest causes of bowel symptoms in young people
| - Functional disorder i.e. no structural or tissue abnormality
45
Symptoms in IBS (2)
1. “Swinging” bowel habit – alternates between constipation & diarrhoea
2. Abdominal pain typically relieved with defecation
Associated symptoms
- Urgency, feeling of incomplete evacuation
- Passage of mucus
- Abdominal bloating
- Excess flatus
May occur after gastroenteritis (post-infective IBS)
46
Associated symptoms in IBS (6)
1. Fatigue
2. Backache, headache
3. Urinary symptoms
4. Dysmenorrhoea, dyspareunia
5. Palpitations
6. Poor sleep quality
Other functional GI symptoms:
- Functional dyspepsia
- Early satiety, post-prandial fullness
- Nausea, vomiting
47
Alarm features in IBS (8)
1. Older patient (over 50, but even 40+ should re-consider other diagnoses)
2. Short history
3. Nocturnal diarrhoea / nocturnal pain
4. Bleeding in stools
5. Iron deficiency
6. Weight loss
7. Vomiting
8. Family history of colon cancer
48
Pathophysiology of IBS (3)
1. Altered gut motility
2. Visceral hypersensitivity
3. Central sensitisation
49
Management of IBS (3)
1. Dietary – Low FODMAP diet
2. Pharmacologic – tailor to diarrhoea- / constipation- / pain predominant
3. Probiotics (may be more useful in post-infective IBS)
50
FODMAPs
Fermentable Oligo-, Di-, Monosaccharides & Polyols
Oligosaccharide’s – fructose & glucose
Disaccharides – lactose
Monosaccharides – fructose
Polyols – sorbitol, mannitol
Eliminate food containing FODMAPs
51
Probiotics
- Some evidence of benefit for probiotics in IBS
| - May be strain-dependent
52
Other considerations in IBS (2)
1. Lifestyle advice
- Regular meals – unhurried – particularly breakfast
- Reduce stress levels
- Adequate sleep
2. Psychological therapies
- Many approaches have been shown to be helpful
- Cognitive behavioural therapy / hypnotherapy
53
Inflammatory Bowel Disease (IBD)
Covers 2 different diseases:
1. Ulcerative colitis (UC)
2. Crohn’s disease (CD)
Involves genetic & environmental factors
54
IBD - Genetics
- 1st degree relatives of IBD patients are 3-20x more likely to have IBD than general population
- Like many genes involved & not fully elucidated
- Very uncommon in certain ethnic groups e.g. Maori, Pacific Island
- But despite the role of genes, important to remember that majority of IBD patients (~85%) do not have family history
55
IBD - Environmental
- Common in “western” industrialised nations
+ Improved living standards – less exposure to enteric infections – less “tolerance” of immune system
Smoking increases risk of Crohn’s disease
Smoking protective for UC
- Often develops within a year of stopping smoking
- Restarting smoking can lead to resolution of inflammation BUT:
* **PLEASE DON’T ADVISE PATIENT TO START SMOKING!!!***
56
IBD - Pathophysiology
- Not fully understood
- Disruption of the integrity of epithelial barrier of the colon
- Certain microbes in the gut may be pathogenic & initiate IBD
57
Crohn's disease
- Any part of the GI tract (most commonly colon & small intestine, but can be stomach, oesophagus, mouth etc)
- Discontinuous inflammation i.e. skip lesions, may spare rectum
- Transmural involvement
- Made worse by smoking
58
Ulcerative colitis
- Colon only
- Continuous inflammation starting at the rectum
- Mucosal involvement only
- Smoking is protective
59
Symptoms in IBD (3)
1. Diarrhoea
2. Bleeding in stools
3. Abdominal pain
Diagnosis of IBD & differentiation between Crohn’s disease & UC require colonoscopy
60
Crohn's disease - other manifestations (3)
Crohn’s can be associated with:
1. Stricturing
2. Fistulising
3. Perianal disease
These do not occur in UC
61
Crohn's disease - stricturing (3)
Stricturing disease:
1. Abdominal pain & distension
2. Vomiting
3. Bowels not opening
62
Crohn's disease - fistulising (2)
Fistulising disease:
1. E.g. Bowel to skin
2. E.g. Bowel to bowel
Fistula – an abnormal connection/tract between the gut & another organ/vesse
63
Crohn's disease - perianal (3)
1. Perianal abscess
2. Perianal fistula
3. Anal fissure
64
Extra-intestinal manifestations of IBD
Eyes:
- Episcleritis
- Uveitis
Kidneys:
- Stones (nephrolithiasis)
- Hydronephrosis
- Fistulae
- UTI
Skin:
- Erythema nodosum
- Pyoderma grangrenosum
Mouth:
- Stomatitis
- Apithous ulcers
Liver:
- Steatosis
Billary tract:
- Gallstones
- Sclerosing cholangitis
Joints:
- Spondylitis
- Sclerosing cholangitis
Joints
- Spondylitis
- Sacroilitis
- Peripheral arthritis
65
Lower GIT - Perianal region: Haemorrhoids & anal fissures
Both most commonly due to constipation
Haemorrhoids:
- External or internal
- Fresh bright bleeding on wiping
Anal fissures:
- Fresh bright bleeding on wiping, often painful defaecation as well
- Very occasionally associated with Crohn’s
66
Rectal bleeding
Colour of blood:
Black – melaena
- Upper GI tract/small intestine
Bright red – on the paper
- Outlet bleeding i.e. perianal causes
Bright red – mixed with stools
- Left colon
Dark red
- Proximal colon i.e. caecum to transverse colon
- Distal
67
Lower GI Tract - Colon cancer
- Rectal bleeding, mixed in with stools & dark
- New change in bowel habit, usually diarrhoea
- Older adult
- Iron deficiency
+ Except in young menstruating women or strict lifelong vegetarian
- Weight loss
