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PHARM 213 Gastrointestinal > 3. Presentation & Pathophysiology of GI Conditions > Flashcards

3. Presentation & Pathophysiology of GI Conditions Flashcards

1
Q

Layers of the GIT (4)

A
  1. Mucosal layer
  2. Submucosal layer
  3. Muscularis layer
  4. Serosa layer
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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
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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
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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
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5
Q

Other contributing mechanisms of GORD (3)

A
  1. Hypotensive LOS i.e. not contracting tight enough
    - Caffeine, alcohol, chocolate, fats
    - Certain medications e.g. beta blockers, nitrates, calcium channel blockers
  2. Hiatus hernia
    - Note: Not all people with hiatus hernia have reflux
    - Relevant, but not main part of the pathophysiology
  3. Impaired oesophageal peristalsis
    - Reduced clearance
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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
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7
Q

Symptoms of GORD (4)

A
  1. Heartburn/chest discomfort
    - Burning sensation or discomfort over the chest
  2. Regurgitation
    - Food or liquid coming back up into the mouth
  3. Sour or bitter taste in mouth
  4. May worse after eating or lying down (e.g. bed time)
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8
Q

Complications of GORD (4)

A
  1. Reflux oesophagitis
  2. Peptic stricture
  3. Barrett’s oesophagus
  4. Cancer – oesophageal adenocarcinoma
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9
Q
  1. 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)
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10
Q
  1. Peptic Stricture
A
  • Prolonged inflammation of oesophageal mucosa by reflux can lead to fibrosis and scarring
  • Dysphagia (difficulty swallowing or food sticking)
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11
Q
  1. 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
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12
Q
  1. 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
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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
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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
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15
Q

Gastric motility (4)

A
  1. Relaxation of fundus (vagovagal reflex)
  2. Contraction of body & antrum
  3. Pylorus contracts
  4. Mixing by retropulsion
  • Fundus acts as a food store
  • Body & antrum mix food
  • Pylorus contracts to limit exit of chyme
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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

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17
Q

Protection of gastric mucosa from acid (5)

A

Protective factors:

  1. Mucous layer
  2. Bicarbonate secretion
  3. Epithelial barrier regenerates rapidly
  4. Prostaglandins
  5. Mucosal blood flow (sweeps hydrogen ions away)
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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)
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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
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20
Q

Peptic ulcer disease (PUD)

A
  • Helicobacter pylori most common
  • Other causes:
    + Aspirin
    + NSAIDs
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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
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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
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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
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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
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25
Q

Functional dyspepsia

A

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
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26
Q

How to treat functional dyspepsia (4)

A
  1. Proton pump inhibitor
  2. Prokinetics e.g. domperidone
  3. Low dose tricylic anti-depressant
  4. Cognitive behavioural therapy/psychotherapy/hypnotherapy
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27
Q

Alarm features associated with dyspepsia (6)

A
  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
Q

Lower GI Tract – Small intestine & colon: Common disorders

A
  • Infection
  • Irritable bowel syndrome (IBS)
  • Functional constipation
  • Coeliac disease
  • Inflammatory bowel disease (IBD):
    + Crohn’s disease & ulcerative colitis
29
Q

Infective gastroenteritis

A

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
Q

Pathogens (3)

A

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
Q

Risk factors for infective gastroenteritis (6)

A
  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
Q

Management of infective gastroenteritis

A

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
Q

Helminthiasis & intestinal worms (4)

A

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
Q

Threadworm/pinworm (Enterobius vermicularis)

A
  • 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
Q

Other causes of pruritis ani

A

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
Q

Bowel habit - Normal?

A

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
Q

Constipation

A

Too slow:

  • Reduced bowel frequency
  • Hard / firm stools
  • Straining
38
Q

Chronic constipation

A

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
Q

Alarm features with constipation (5)

A
  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
Q

Management of functional constipation (4)

A
  1. Fibre
  2. Fluid intake
  3. Lifestyle
  4. Laxatives – osmotic preferable over stimulant
41
Q

Diarrhoea

A

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
Q

Chronic diarrhoea causes (4)

A

Long list of causes including:

  1. Functional (as part of irritable bowel syndrome)
  2. Inflammatory bowel disease
  3. Coeliac disease
  4. Medications
43
Q

Alarm features with diarrhoea (5)

A
  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
Q

Irritable bowel syndrome (IBS)

A
  • Commonest causes of bowel symptoms in young people

- Functional disorder i.e. no structural or tissue abnormality

45
Q

Symptoms in IBS (2)

A
  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
Q

Associated symptoms in IBS (6)

A
  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
Q

Alarm features in IBS (8)

A
  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
Q

Pathophysiology of IBS (3)

A
  1. Altered gut motility
  2. Visceral hypersensitivity
  3. Central sensitisation
49
Q

Management of IBS (3)

A
  1. Dietary – Low FODMAP diet
  2. Pharmacologic – tailor to diarrhoea- / constipation- / pain predominant
  3. Probiotics (may be more useful in post-infective IBS)
50
Q

FODMAPs

A

Fermentable Oligo-, Di-, Monosaccharides & Polyols

Oligosaccharide’s – fructose & glucose

Disaccharides – lactose

Monosaccharides – fructose

Polyols – sorbitol, mannitol

Eliminate food containing FODMAPs

51
Q

Probiotics

A
  • Some evidence of benefit for probiotics in IBS

- May be strain-dependent

52
Q

Other considerations in IBS (2)

A
  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
Q

Inflammatory Bowel Disease (IBD)

A

Covers 2 different diseases:

  1. Ulcerative colitis (UC)
  2. Crohn’s disease (CD)

Involves genetic & environmental factors

54
Q

IBD - Genetics

A
  • 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
Q

IBD - Environmental

A
  • 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
Q

IBD - Pathophysiology

A
  • Not fully understood
  • Disruption of the integrity of epithelial barrier of the colon
  • Certain microbes in the gut may be pathogenic & initiate IBD
57
Q

Crohn’s disease

A
  • 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
Q

Ulcerative colitis

A
  • Colon only
  • Continuous inflammation starting at the rectum
  • Mucosal involvement only
  • Smoking is protective
59
Q

Symptoms in IBD (3)

A
  1. Diarrhoea
  2. Bleeding in stools
  3. Abdominal pain

Diagnosis of IBD & differentiation between Crohn’s disease & UC require colonoscopy

60
Q

Crohn’s disease - other manifestations (3)

A

Crohn’s can be associated with:

  1. Stricturing
  2. Fistulising
  3. Perianal disease

These do not occur in UC

61
Q

Crohn’s disease - stricturing (3)

A

Stricturing disease:

  1. Abdominal pain & distension
  2. Vomiting
  3. Bowels not opening
62
Q

Crohn’s disease - fistulising (2)

A

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
Q

Crohn’s disease - perianal (3)

A
  1. Perianal abscess
  2. Perianal fistula
  3. Anal fissure
64
Q

Extra-intestinal manifestations of IBD

A

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
Q

Lower GIT - Perianal region: Haemorrhoids & anal fissures

A

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
Q

Rectal bleeding

A

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
Q

Lower GI Tract - Colon cancer

A
  • 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

PHARM 213 Gastrointestinal (9 decks)

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