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Life Maintenance > GI Histopathology and Visceral Afferents > Flashcards

GI Histopathology and Visceral Afferents Flashcards

1
Q

What is the difference between haematoxylin and Eosin stains?

A

Haematoxylin

  • Purple-blue basic stain
  • Stains acidic macromolecules , ie DNA, RNA- nuclei

Eosin

  • Pink acidic stain
  • Stains basic macromolecules, ie cytoplasm of cells, collagen
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2
Q

Special stains

A

Perodic acid Schiff (PAS) +/- diastase- stains glycogen
Alcian blue- mucin
Masson’s trichrome- collagen etc
Perl’s- stains iron

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3
Q

Immunohistochemistry

A

Modern technique for staining

First described by Coons in 1941

Relies on Antigen (Ag)- Antibody (Ab) link

Used to label specific antigens

  • indirect method, primary antibody targets antigen of interest and secondary antibody attaches to this- enzyme attaches to secondary antibody converts substrate into coloured product (diaminobenzidine- brown)
  • direct where enzyme or fluorescent molecule attached directly to antibody but indirect means multiple secondary antibodies attach to primary = amplification

Primarily diagnostic use
Increasingly used to guide therapy

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4
Q

Epithelium structure

A
  • Closely packed cells, with little to no extracellular material
  • Form membranes or glands
  • Epithelium separated from connective tissue by basement membrane
  • Squamous, columnar, cuboidal cells
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5
Q

Epithelium functions

A

Protection : skin

Secretion/ excretion

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6
Q

Epithelium types

A

Simple (one cell layer)

Stratified ( more than one cell layer)

Pseudo-stratified

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7
Q

What tissue is this?

A

Simple epithelium

lots of pin cytoplasm because of lots of mitochondria

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8
Q

What tissue is this?

A

Stratified epithelium

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9
Q

What tissue is this?

A

Transitional epithelium (urothelium)

Has ability to stretch and maintain a tight barrier to prevent urine leaving the bladder

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10
Q

Connective tissue structure

A

Composed of

  • Extracellular matrix
  • A few cells
  • Provides structural and metabolic support

Extracellular matrix

  • Fibres (collagen , elastin)
  • Amorphous ground substance (gel like matrix)
  • Extracellular fluid
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11
Q

Connective tissue cell types

A

Fibroblasts
Adipocytes
Macrophages
Lymphoid cells ( plasma cells, leucocytes)

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12
Q

What tissue is this?

Label diagram

A

Connective tissue

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13
Q

What type of tissue is adipose tissue?

A

Connective tissue

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14
Q

What type of tissue is this?

A

Adipose tissue

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15
Q

What type of tissue is cartilage?

A

Connective tissue

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16
Q

What tissue is this?

A

Cartilage

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17
Q

What cartilage type:
articulates bone surfaces?
is in the ear?
is in intervertebral discs?

A

Hyaline cartilage articulates bone surfaces

Elastic cartilage in ear

Fibrocartilage in intervertebral discs

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18
Q

What cells produce cartilage?

A

Chondrocytes (found in lacunae)

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19
Q

What are the bone cells that sit in lacunae in the bone matrix?

A

Osteocytes

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20
Q

Bone composition

A

Protein matrix containing collagen
Mineral substances - calcium hydroxyapatite laid down on matrix giving it calcified supportive structure

Osteoclasts also present to reabsorb bone

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21
Q

Where does haematopoiesis occur?

A

Bone marrow

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22
Q

Skeletal muscle

A

Attached to skeleton
Long cylindrical fibres with an eccentric nuclei
Striated

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23
Q

Smooth muscle

A

Present in hollow viscous organs
Shorter cells with centrally placed nucleus
No striations

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24
Q

Cardiac muscle

A

Striated

Centrally located nucleus

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25
Q

Identify which muscle type each one is

A
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26
Q

Nervous tissue: CNS vs PNS

A 
CNS:
Neurons
Supporting cells
Oligodendroglia, astrocytes 
Schwann cells, microglia

PNS:
Bundles of parallel elongated fibres
Wavy, zig zag configuration

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27
Q

What tissue is this?

A

Nervous tissue

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28
Q

What tissue is this?

A
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29
Q

Histopathology

A

Microscopic examination of cells and tissue to study disease

The gold standard diagnostic technique

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30
Q

Metaplasia

A

Transformation of one differentiated cell type to another differentiated cell type

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31
Q

Dysplasia

A

An abnormality of development

Epithelial dysplasia- loss of maturation

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32
Q

Structure of wall of GI tract

A
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33
Q

Structure of the wall of GI tract

A
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34
Q

What lines normal oesophagus?

A

Pale pink squamous mucosal lining

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35
Q

Squamous mucosa structure

A
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36
Q

What is the deepest layer of normal oesophagus lined with?

A

Basal cells (single layer) including stem cells

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37
Q

Features of normal oesophageal squamous epithelium

A
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38
Q

Causes of impaired oesophageal sphincter control in GORD/reflux oesophagitis?

A 
Hiatus hernia
Obesity/pregnancy
Gastric distension by food/gas
Stress
Alcohol and tobacco/drugs
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39
Q

What does acid gastric contents damage?

A

Unprotected squamous mucosa

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40
Q

Acidic damage to unprotected squamous mucosa causes what?

A

infiltration of the damaged surface epithelium by neutrophil polymorphs and eosinophils

basal cell hyperplasia as epithelium proliferates to replace damaged cells

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41
Q

What does reddened patches on lower oesophagus mean?

A

Inflammation, secondary to reflux of acidic gastric contents

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42
Q

What happens to basal cells in GORD/reflux oesophagitis?

A

Hyperplasia

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43
Q

Complications of GORD

A

Peptic ulceration, i.e. acid-induced benign ulceration

Replacement of squamous mucosa by glandular mucosa.
Columnar metaplasia = Barrett’s oesophagus

Development of dysplasia in Barrett’s oesophagus

Development of adenocarcinoma in Barrett’s oesophagus

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44
Q

What happens to mucosa in an ulcer?

A

Complete break in mucosa, discontinuation in mucosa. Inflammatory slough with fibrin on surface

Base of ulcer formed from granulation tissue consist of early fibrosis with proliferation of new capillaries (later forms fibrosis or scar tissue)

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45
Q

What problems can arise from a healing peptic ulcer?

A

As peptic ulcer heals scar tissue can form leading to peptic stricture in oesophagus

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46
Q

Barrett’s oesophagus

A

Complication of GORD

The squamous mucosa undergoes metaplasia from the normal squamous epithelium to columnar epithelium (glandular type epithelium)

(acid reflux causes metaplasia)

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47
Q

Metaplasia and reversability

A

Metaplasia is the reversible replacement of one mature type of epithelium by another in response to adverse circumstances.

Columnar cell metaplasia in oesophagus = Barrett’s oesophagus

2º v(secondary) to GORD/reflux oesophagitis

Mucus barrier of columnar epithelium protects against acid

Metaplasia is reversible if the stimulus is removed.

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48
Q

What replaces squamous epithelium in Barrett’s oesophagus?

A

Metaplastic columnar epithelium

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49
Q

What does Barrett’s metaplasia consist of?

A

Barrett’s metaplasia is often a mixture of non-specialised gastric-type mucosa and intestinal metaplasia
Intestinal metaplasia with goblet cells

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50
Q

Dysplasia

A

Premalignant change within the epithelium

Characterised by:
Impaired cell differentiation : disorganised, often failing to mature towards surface
Atypical nuclear features, eg pleomorphism
Increased numbers of mitoses

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51
Q

Dysplasia in Barrett’s oesophagus

A

Dysplasia in Barrett’s oesophagus: surface epithelium shows multilayering of nuclei, with hyperchromatism, pleomorphism and increased mitoses

Non-dysplastic metaplastic columnar mucosa in Barrett’s oesophagus

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52
Q

How does carcinoma of oesophagus present in Barrett’s oesophagus?

A

Carcinoma of oesophagus presents with dysphagia due to luminal narrowing and infiltration of the wall, inhibiting peristalsis

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53
Q

What are the 2 types of adenocarcinoma of oesophagus?

A

Intestinal type formed by irregular glands

Diffuse type (signet ring carcinoma)

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54
Q

Normal squamous vs dysplasia squamous

A

Normal squamous mucosa shows orderly maturation from the basal layer to the surface.

Squamous epithelial dysplasia in the oesophagus. Disordered maturation and increased mitotic figures.

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55
Q

Where does squamous cell carcinoma typically occur?

A

Mid or upper oesophagus

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56
Q

Where does adenocarcinoma of oesophagus typically occur?

A

lower oesophagus and GOJ (gastroesophageal junction)

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57
Q
A
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58
Q
A
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59
Q

What mucosa is on the surface of the body and fundus?

A

Specialised gastric mucosa

Mucous neck cells secrete a blanket of mucus over the surface which protects it from digestion by enzymes and acid.

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60
Q

2 types of specialised body-type gastric mucosa

A

Parietal cells (pink-staining) secrete gastric acid

Chief cells (purple-staining) secrete pepsinogen, which is activated by acid in the lumen of the stomach to form the active protease enzyme pepsin.

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61
Q

What cells are found on the antrum and pylorus?

A

Non-specialised gastric mucosa

Glands formed by mucus producing cells

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62
Q

Protective mechanisms in stomach

A

MUCUS BLANKET continually secreted by mucus neck cells

BICARBONATE BUFFER LAYER secreted by epithelial cells in gastric neck/isthmus

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63
Q

What can interfere with the mucus blanket?

A

Drugs, alcohol and H. pylori infection

Mucus blanket relies on intact mucin neck cells for production so any inflammatory stimulus will interfere

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64
Q

What can interfere with bicarbonate buffer layer?

A

Bicarbonate (HCO3-) secretion is stimulated by prostaglandins, produced from arachidonic acid by COX pathway, inhibited by NSAIDs

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65
Q

How does pepsin form?

A

Pepsin forms from pepsinogen in acid-rich environment

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66
Q

What do parietal cells and chief cells secrete?

A

Parietal: acid

Chief: pepsinogen, not activated until pH is low

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67
Q

Gastritis pathology

A

Infiltration by acute inflammatory cells like neutrophils and chronic inflammatory cells like plasma cells and lymphocytes

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68
Q

2 main causes of gastritis

A

NSAIDs and H. pylori

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69
Q

What is a consequence of gastritis?

A

Gastric peptic ulcer in stomach
Duodenal peptic ulcer in duodenum

Peptic-type ulceration is due to acid.Seen in oesophagus, stomach and duodenum

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70
Q

Complications of peptic ulcers in stomach or duodenum

A
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71
Q

Intestinal-type adenocarcinoma vs ulcerated adenocarcinoma

A

Intestinal-type adenocarcinomas usually present as ulcers or polypoid tumours.

Ulcerated adenocarcinoma has a ‘rolled’ everted edge, unlike the overhanging edge of benign peptic ulcer

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72
Q

Gastric peptic ulcer vs ulcerated gastric adenocarcinoma

A

Gastric peptic ulcer:
surface has granulation tissue with inflammatory slough, NO epithelial cells in submucosa

Adenocarcinoma:
nests of irregular glands invading from mucosa into submucosa and into muscularis propia

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73
Q

Gastric peptic ulcer vs ulcerated gastric adenocarcinoma

A

Gastric peptic ulcer:
surface has granulation tissue with inflammatory slough, NO epithelial cells in submucosa

Adenocarcinoma:
nests of irregular glands invading from mucosa into submucosa and into muscularis propia

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74
Q

Diffuse (signet-ring cell) type adenocarcinoma presentation in stomach

A

Stomach often shrunken, thickened and non-distensile; patient may present with early satiety.

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75
Q

Somatic pain

A

musculoskeletal (joint pain, myofascial pain), cutaneous; often well localized

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76
Q

Visceral pain

A

hollow organs and smooth muscle; usually referred

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77
Q

Neuropathic

A

pain initiated or caused by a primary lesion or disease in the somatosensory nervous system.

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78
Q

Hollow and solid organs

A

Not all internal organs sensitive to pain e.g. liver, lungs, kidneys – no nociceptors

Stretching of hollow viscera such as gall bladder, ureters, colon can cause excruciating pain
no close relationship between severity of damage and severity of pain

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79
Q

Extrinsic sensory neurones work with what other cells?

A

Immune cells in gut wall

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80
Q

Interstitial cells of Cajal

A

Pacemaker cells

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81
Q

Sensations from the gut

A 
Oesophageal distension
Gastric distension – fullness
Nutrient density in stomach/duodenum
Nausea-toxins or excess nutrients
Movement of gas
Pain
Awareness of rectal content
Urgency
82
Q

Visceral afferent pathways in the GI tract

A

Vagal afferents
Thoracolumbar (splanchnic) afferents (pain)
Pelvic afferents (gut)
Enteric afferents - viscerofugal neurons

83
Q

How many different types of sensory neurones give rise to sensation from the gut?

A

Serosal/Muscular/Mesenteric
– distension/contraction – mechanoreceptors

Mucosal – entero-endocrine mediators

Musculo-mucosal 
Vascular afferents (serosal)
84
Q

What is the location of the sensory neurons of the gut?

A

Intra-ganglionic – low threshold mechanoreceptors primarily in vagal and pelvic pathways (longitudinal muscle)

Intramuscular afferents – mechanosensitive (muscular propria)

Mucosal afferents – mucosal distortion and entero-endocrine cell mediators (vagal and spinal) (mucosa)

Muscular-mucosal – mucosal stroking and distension/contraction – in vagal and pelvic pathways (submucosa)

Vascular afferents – on extramural and intramural blood vessels – mechano-nociceptors – splanchnic and pelvic pathways (submucosa to longitudinal muscle)

Entero-viscerofugal – interneurons with mechanosensitivity (LM)

85
Q

Visceral pain in clinical practice- pain caused by:
‘structural’ conditions?
‘functional’ conditions?

A

Pain caused by ‘structural’ conditions

  • Inflammatory e.g. acid-peptic disease,
  • Neoplastic

Pain caused by ‘functional’ conditions

  • Irritable bowel syndrome (include bloating)
  • Functional dyspepsia (include nausea)
86
Q

Stimuli for visceral pain

A 
Hollow organ distension
Traction
Ischaemia
Acid/Irritant chemicals
Inflammation
Electrical stimulation
‘pinching’ does not cause pain except when hyperalgesic
87
Q

Somatic abdominal pain features

A

‘Painful rib’ syndrome
Spinal pain
Pain from abdominal wall or inguinal ligaments
Constant, can be sharp and momentary with movement or straining
Well localised
Unaffected by food, defaecation
Affected by position, movement, straining
Localised Tenderness, reproduces pain

Subluxation of costal cartiledge tips causing impingement of the intercostal nerves

88
Q

Example of visceral pain becoming somatic

A

Acute appendicitis:

  • In early phase visceral intestinal pain – central abdominal, colicky
  • With onset of inflammation of parietal peritoneum, somatic pain localised to RIF
  • Worse with movement and straining
  • Tenderness at McBurney’s point
89
Q

Treatment of visceral pain

A
  1. Treat disease e.g. peptic ulcer
  2. Anti-spasmodics e.g. for irritable bowel syndrome
  3. For visceral hypersensitivity use tricyclics
    e. g. Amitryptiline
  4. Used in sub-anti-depressant doses
  5. Start at low dose e.g. 10 mg nocte and step up
  6. Main problem is sedation – take at 6 pm
90
Q

Hyper vigilance and pain

A

Mild pain can become difficult to bear when patients are worried about it – leads to anxiety, panic etc
Pain may not be noticed when engaged in other activities e.g. Watching TV
‘Painful rib’ syndrome – continuous pain day and night. Many patients cope with it much better once they understand it is not serious. Analogous to rheumatism

91
Q

Achalasia

A

An oesophageal motility disorder causing dysphagia

Degeneration of ganglion in myenteric plexus in oesophageal wall leading to motility disorder:

  • Aperistalsis
  • Incomplete lower sphincter relaxation
  • Treat by myotomy, pneumatic dilatation or botulinum toxin injection
92
Q

Gastro-oesophageal reflux

A

Incompetent lower oesophageal sphincter, but resting pressure may be normal

Gastric acid secretion usually within normal limits

Oesophagitis seen at endoscopy but normal appearances in non-erosive gastro-oesophageal reflux

Ambulatory lower oesophageal pH monitoring

93
Q

Oesophageal exposure to acid causes…

A

Hypersensitivity

(hyperalgesia aka primary, local OR allodynia aka to non painful stimuli OR, secondary hyperalgesia aka generalised)

94
Q

Hyperalgesia

A

an increased sensitivity to feeling pain eg overuse of opiods ie exaggerated response

95
Q

Allodynia

A

things that don’t normally cause pain eg very sensitive to touch/temperature

96
Q

Secondary hyperalgesia

A

generalized response not just at the area of injury

97
Q

Ion channels in the oesophagus

A
  1. Transient Receptor Potential Vanilloid-1 (TRPV-1)
  2. Acid-Sensing Ion Channel (ASIC)

Acid excites primary sensory neurons by activating TRPV1 and ASIC – leads to release of pro-inflammatory mediators and neurogenic inflammation

Sensitive to mechanical, electrical and thermal stimuli

98
Q

Erosive reflux disease vs NERD

A

Erosive- mucosal damage

NERD- no mucosal damage

99
Q

What organs does Gi tract share neural pathways with?

A

Lungs and trachea

100
Q

Using pH testing on a patient with GORD the result is abnormal what is the likely diagnosis?

A

NERD

Posiitve result- abnormal acid exposure

101
Q

What would pH result be if a patient with GORD had functional heartburn?

A

Normal pH test

May have symptoms associated with pH changes- hypersensitive oesophagus or just functional heartburn

102
Q

Gastric motility and secretion

A

Fundus – accommodates
Antrum – grinding effect
Food boluses converted into chyme
Greasy and rich food delays gastric emptying
Stomach secretes acid and pepsin
Vagus, gastrin (secreted by G cells) and acetylcholine promotes acid secretion
Proton pump - final common pathway for acid secretion

103
Q

Delayed gastric emptying

A

Often occurs in dysmotility type dyspepsia, sometimes associated with nausea, vomiting and weight loss
Severe gastric emptying delay in gastro-paresis, often diabetic, sometimes post-infective
Pro-kinetic drugs: domperidone, metoclopramide also helps nausea and vomiting
Isotope gastric emptying study

104
Q

IBS demographics

A 
10-15% of the population
30% consult a physician
Greater anxiety, lower quality of life
Female preponderance
No excess mortality
Rome and Manning Criteria
105
Q

Rome IV criteria

A

Recurrent abdominal pain, on average, at least 1 day/week in the last 3 months, associated with two or more of the following criteria:

Related to defecation
Associated with a change in frequency of stool
Associated with a change in form (appearance) of stool

Disorders of gut-brain interaction
Related to:
- Motility disturbance
- Visceral hypersensitivity
- Altered mucosal and immune function
- Altered gut microbiota
- Altered CNS processing
106
Q

IBS and abnormal perception of normal stimuli

A

Distension in IBS -> abnormal sensory response, pain, urgency, feeling unwell

normal sensory stimulus giving rise to different sensation

increases with increasing distension (higher pressure = more sensitive to discomfort)

107
Q

Importance of physician-patient interaction

A
108
Q

IBS phenotypes

A

IBS with constipation >25% hard stools, <25% loose stools

IBS mixed - both hard and loose stools

IBS with diarrhoea >25% loose stools, <25% hard stools

109
Q

Constipation

A

Many possible causes: low fibre diet, medications such as opiates, hypercalcaemia, hypothyroidism
Chronic constipation not a symptom of colon cancer
Does not produce toxins, ill health or increase risk of colon cancer
Functional types: colonic inertia – slow transit (can assess by marker studies), pelvic floor dys-synergia: pelvic muscles do not relax with defaecation
Management similar for both types of constipation

110
Q

Constipation demographics

A

More common in lower socioeconomic class
Less fibre and less exercise
F:M – 2.2:1

110
Q

Constipation demographics

A

More common in lower socioeconomic class
Less fibre and less exercise
F:M – 2.2:1

111
Q

Beneficial diet for constipation

A

Diet:
Meta-analyses
- Bran – less effect if constipated
- Ispaghula

RCTs

  • Prunes (sorbitol)
  • Kiwifruit
  • Vegetable and wholegrain powder
  • Fruit and fibre to porridge
112
Q

What is the most effective osmotic laxative?

A

Macrogol (polyethylene glycol) more effective and better tolerated than lactulose

Macrogol

  • Proven efficacy in long term treatment
  • Improved stool frequency
  • Improved pain
  • Less need for other laxatives

SE – diarrhoea, bloating

113
Q

First line laxatives for:
Osmotic?
Stimulant?
Stool softeners?

A

Osmotic:

  • Macrogol
  • Avoid lactulose

Stimulant

  • Sodium picosulphate
  • Bisacodyl
  • Senna

Stool softeners
- Sodium docusate

SE – osmotic – bloating
SE – stimulant - cramps

114
Q

Individualised diet for patients with IBS

A 
Regular, small meals
Fat reduction
Caffeine
Reduce lactose and fructose
Reduce gas-producing foods
Modify soluble/insoluble fibre
Reduce wheat
Low FODMAP diet (reduces bifidobacteria)
115
Q

What do we know about bifidobacteria in relation to helping IBS patients?

A

Gas related symptoms

Inverse relationship between pain and bifidobacteria

116
Q 
Sites of abdominal pain- what organs are implicated in:
Chest
Upper
Mid
Lower
Back pain?
A
  • Chest - oesophagus
  • Upper- oesophagus, stomach, duodenum, pancreas, gallbladder, colon
  • Mid – Small intestine
  • Lower – Colon, gynaecological

Radiation to back with severe pain, biliary pain, pancreatic pain, spinal pain

117
Q

Visceral vs non-visceral pain

A

Visceral pain lasts minutes/hours, intense can come and go

Non visceral pain well localised, lasts for seconds or constant
Exacerbated by movement, coughing, straining

Nerve pains- shooting and needle-like, sharp

Musculoskeletal- spinal, painful rib syndrome, pain over ligaments, bones and joints

118
Q

Character and severity of upper abdominal pain:
Acid peptic pain?
Intestinal pain?
Biliary colic?

A

Acid peptic: burning or dull (mild or moderately severe)

Intestinal/colonic: colicky (extremely severe, bad or worse than labour pains)

Biliary/pancreatic pain: constant or colicky (extremely severe)

119
Q

Associated symptoms with oesophageal pain

A

heartburn, regurgitation, dysphagia, odynophagia

120
Q

Associated symptoms with gastric pain

A

early satiety, post-prandial fullness, nausea

121
Q

Associated symptoms with biliary pain

A

dark urine, pale stools, jaundice

122
Q

Associated symptoms with colonic pain

A

diarrhoea, constipation, distension

123
Q

Causes of upper abdominal pain

A
  • gastro-oesophageal reflux
  • functional dyspepsia
  • gastric ulcer/duodenal ulcer
  • ca stomach/oesophagus/pancreas/liver
  • cholelithiasis
  • acute or chronic pancreatitis
  • irritable bowel
  • Non-visceral pain: musculo-skeletal, neuralgic, cardiac
  • More than one cause of pain
124
Q 
Exacerbating/aggravating factors in:
Oesophagitis
Gastro-oesophageal reflux
Peptic ulcer
IBS
A
  • Oesophagitis – exacerbated by swallowing
  • Gastro-oesophageal reflux - exacerbated by food, drink, lying down, bending over, relieved by antacids, milk, sitting up
  • Peptic ulcer – nocturnal, worse on hunger, improved by food and antacids
  • Irritable bowel syndrome – pain gives an urge to defaecate, relieved by defaecation, distension
125
Q

Investigations for abdominal pain

A

• ‘Test and treat’ for Helicobacter (if no alarm
symptoms)
• Blood count, ESR, LFTs, amylase
• Plain X ray, urgent CT, if acute abdomen
suspected
• Ultrasound
• CT
• Upper endoscopy
• Colonoscopy- not normally indicated for
abdominal pain
• Lower oesophageal pH study

126
Q

In primary care, dyspepsia is defined as:

A
  • recurrent epigastric pain, heartburn or acid regurgitation, with or without bloating, nausea or vomiting
  • Also… postprandial fullness, early satiation and heartburn…
  • GORD and dyspepsia symptoms often overlap
  • Lower quality of life than pts with DM/CHF1
127
Q

Initial presentation of dyspepsia

A
  • Differential Diagnosis – cardiac and biliary disease
  • FBC
  • Medication review – calcium antagonists, nitrates, theophyllines, bisphosphonates, corticosteroids and NSAID’s
  • Offer H. pylori ‘test and treat’ to people with dyspepsia.
128
Q

What to do if initial therapy for dyspeptic patient doesn’t work?

A

• H.Pylori Eradication
– 83% had Symptoms (Sx) at 12 mths
– 34% incurred further costs

• PPI Therapy (proton pump inhibitor)
– 84.5% had Sx at 12mths
– 33% incurred further costs

129
Q

What are the predictors of a positive response to a 4 week trial of PPI?

A 
• Fewer days of Sx during the 1st week of 
treatment
• Age>40
• Symptoms > 3 mths
• High Score for heartburn at baseline
• Low Score for Epigastric Pain, bloating, 
diarrhoea at baseline
• Low impairment of vitality at baseline
130
Q

CASE:
• 46 year old man, 6 week history of ‘indigestion’
• FBC, LFT’s, ECG normal
• Medication review – calcium antagonists, nitrates, theophyllines, bisphosphonates, corticosteroids and NSAID’s – none taken
• H. pylori Stool Ag - negative

Persistent symptoms
• Would you send him for an OGD?
• What are the indications for a TWR OGD (2 week rule GI endoscopy)?

A

CT
If expect a cancer, investigation done much more rapidly eg TWR- doesn’t seem to be the case here
Patient is under 5 so not seen as urgent to do this

131
Q

When would you want to perform URGENT direct access upper GI endoscopy TWR?

A

dysphagia

or aged 55 and over with WEIGHT LOSS and any of the following:
• upper abdominal pain
• reflux
• dyspepsia

(weight loss may be an indication of cancer- urgent)

132
Q

Reflux oesophagitis grades

A

A - 1 or more mucosal breaks no longer than 5mm, does not extend between tops of 2 mucosal folds

B - 1 or more mucosal breaks more than 5mm long, does not extend between tops of 2 mucosal folds

C - 1 or more mucosal breaks continuous between tops of 2 or more mucosal folds, involves less than 75% of circumference

D - 1 or more mucosal break involving 75% at least of oesophageal circumference

133
Q

Duration of treatment for someone with severe oesophagitis (Grade C/D)?

A

8-12 weeks

PPI works best over 8 week period
Healing lasts up to 12 weeks

134
Q

While being taken, when are PPIs more effective?

A

Better acid suppression when taken BEFORE a meal

135
Q

If patient is still symptomatic after PPI therapy, what is added in?

A

Add in PPI BID (twice daily) and H2 receptor antagonist

Improves gastric acid control and decreases nocturnal acid breakthrough (bc taken morning and night)

136
Q

What do do if patient has refractory reflux symptoms?

A

• Step 1 check adherence
• Step 2 confirm diagnosis
– Does the patent really have GORD?
do endoscopy if necessary

What % of patients with PPI refractory
reflux symptoms (heartburn and
regurgitation) do not have GORD?
– 50%

137
Q

When is surgery considered for GORD?

A

If PPIs not tolerated (cause diarrhoea, headaches, dizziness, tiredness) or patient has concerns about long term use of tablets

138
Q

Montreal classification of GORD

A
139
Q

Alarm symptoms in patients with dyspepsia

A
  • Anorexia
  • Weight loss
  • Persistent vomiting
  • Anaemia
  • Haematemesis and melaena
  • Abdominal mass
140
Q

Treatment of GORD

A

• Lifestyle
– Wt loss, elevation of head of bed, smoking, meal times, (CBT, psychological therapies in dyspepsia)

• Medical
– Antacids, alginates, H2RA,PPI, prokinetics

• Surgical
– Fundoplication

• New endoscopic and surgical techniques

141
Q

Management of gastro-oesophageal reflux disease (GORD)

A

• Lifestyle and postural measures:
- Avoid alcohol, smoking, greasy food, caffeine,
weight reduction
- Small meals, eat and drink separately
- No food or drink for 3 hours before going to bed
- Elevate the head of the bed

  • Pharmacological treatment - PPI
  • (Endoscopic treatment)
  • Fundoplication
142
Q

Grade A/B vs Grade C/D treatment

A

Non-erosive, Grade A and B – treat
symptomatically

Grade C and D – probably need long-
term treatment

When it does heal some patients will habe Barrett’s oesophagus- 0.5% annual risk of adenocarcinoma, endoscopy to look for dysplasia

143
Q

Laproscopic nissen fundoplication

A 
• Most common procedure
• Under general anaesthetic
• Upper portion of stomach is wrapped 
around distal oesophagus
• Common side effects include:
– dysphagia
– belching 
– bloating 
– flatulence
144
Q

Stretta procedure

A

Augment oesophageal sphincter and increase barrier function of lower sphincter

145
Q

LINX procedure

A

Metallic bead wrapped around lower sphincter to augment barrier function

146
Q

Peptic ulcer

A
  • Gastric or duodenal
  • Most cases due to H pylori infection or aspirin/NSAIDs
  • ‘No acid, no ulcer’: reduction in gastric acid heals ulcers
  • Can be uncomplicated, Bleeding or perforated
  • Gastric ulcer can be malignant: need follow-up to healing, but not duodenal ulcer won’t be
147
Q

Why do gastric ulcers need follow up?

A

They can be malignant (cancerous), unlike duodenal ulcers

148
Q

Gastric vs duodenal ulcer effects on patient sleep and meals

A
149
Q

Treatment of peptic ulcer

A
  • Treat Underlying Cause: H pylori infection or aspirin/NSAIDs
  • Acid Suppression – PPI
  • Gastric ulcer to be followed up to healing, not necessary for duodenal ulcer
  • Check for Helicobacter eradication if history of complications
  • Bleeding ulcer – maintain haemodynamic stability, endoscopic treatment
  • Perforated ulcer - surgery
150
Q

What abdominal pain is H pylori infection associated with?

A
  • H pylori infection associated with peptic ulcer which can be cured by antibiotic treatment
  • Most patients with H pylori infection do not have ulcer, only gastritis. Some have dyspepsia.
  • Dyspepsia cured by treatment of H pylori infection in <10% of patients with functional dyspepsia and H pylori.
151
Q

Barrett’s BSG guidelines 2014

A 
BO occurs in patients with longstanding 
reflux symptoms (perhaps >10 years) 
But screening for BO not routinely justified 
Only consider if ≥3 risk factors: 
• Males
• Obese individuals
• those aged >50
• Caucasian
• FH of Barrett’s or oesophageal ca, 
• Smoking
152
Q

What in OGD would guide management of Barrett’s oesophagus?

A

Length of lining of oesophagus

Prague classification:
Circumference length = C number
Maximum length = M number

image: C3M5

153
Q

Surveillance intervals BSG guidelines 2014 for Barrett’s oesophagus- how often to survey the patients?

A

Take into account two endoscopic factors:
presence/absence of Intestinal Metaplasia and length of segment:

• Without intestinal metaplasia and <3cm –
single repeat endoscopy in 3-5 years

• With intestinal metaplasia:
<3 cm - 3-5 yearly
>3 cm – every 2-3 years

• Patient co-morbidity and preference

154
Q

Where are pre-ganglionic parasympathetic fibres found?

A

Brainstem cranial nerves

Sacral S2-S4

155
Q

What are the parasympathetic pre ganglionic nerves in the brainstem?

A

3- oculomotor
7- facial
9- glossopharyngeal
10- vagus

156
Q

Length of parasympathetic pre ganglia?

A

LONG

157
Q

Length of parasympathetic post-ganglionic fibres?

A

SHORT (close to end organs)

158
Q

What neurotransmitter is released at parasympathetic post ganglionic fibres (at the end organ)?

A

Acetylcholine at muscarinic receptors

159
Q

What neurotransmitter is released at parasympathetic pre ganglionic fibres?

A

Acetylcholine at nicotinic receptors

160
Q

In the heart, stimulation of vagus nerve releases what neurotransmitter acting at what receptor?

A

Acetylcholine

at M2 receptors

161
Q

Where are M2 receptors found?

A

SA node

AV node

162
Q

In the heart what happens when the vagus nerve is stimulated?

A

Stimulation of vagus nerve releases Ach which acts at M2 receptors

↓ Pacemaker potential frequency at SA node leading to  in heart rate

↓ Electrical conduction through atria-ventricular node
to balance ↓ heart rate to contraction

Using : CO = HR x SV

Stimulation of vagus nerve (↓ HR) will DECREASE CARDIAC OUTPUT

163
Q

Parasympathetic nerves in the heart do NOT…

A

do not innervate ventricles, most blood vessels -> do not affect contractility (SV) or TPR

164
Q

What is the exception to parasympathetic not innervating blood vessels?

A

Exception : male genitalia, where release of NO (not Ach) causes dilatation of vessels to cause erection

165
Q

How does stimulation of Mus receptors produces reduction in HR?

A

Pacemaker cells have hyperpolarised Na channel (If) -> hyperpolarisation, then repolarisation influx of Na depolarises membrane and strikes up another AP

Parasympathetic stimulates M2 receptors = activation of GPCRs (Gi class)

Gi causes inhibition of Adenylate cyclase → decreased conversion of ATP to cAMP → less cAMP = ↓ If current = ↓ pacemaker potentials in SA node → reduced HR

166
Q

How do drugs increase heart rate?

A

Drugs that inhibit Mus receptors can increase HR by inhibiting parasympathetic action

Mus antagonist, e.g. Atropine used to  HR following sinus bradycardia after MI

Caution
Tachycardia - potential side effect of Mus antagonists given for other reasons

167
Q

Muscarinic agonists

A

Mus agonists, e.g. Bethanechol, used to treat urinary incontinence
may induce bradycardia

168
Q

What do parasympathetic nerves regulate in the eye?

A

Pupil diameter
Intra-ocular pressure
Accommodation (focusing)

169
Q

How do parasympathetic nerves regulate pupil diameter

A

Stimulation of M3 receptors lead to constriction of the circular smooth muscle of the iris (constrictor pupillae), constrict of the pupil (miosis)

170
Q

How do parasympathetic nerves regulate intra-ocular pressure?

A

Constriction of the pupil (M3) has a secondary action on opening the canal of Schlemm at the side of the pupil
Drains aqueous humour from eye, reducing pressure within the eye

171
Q

Action of muscarinic agonists vs antagonists on parasympathetic nerves in eye

A

Mus agonist, e.g. Pilocarpine - lowers intraocular pressure in glaucoma

Mus antagonists – dilate pupil to examine retina

Eye drops have less systemic side effects

172
Q

Distance vision mechanism

A

Ciliary muscle relaxed
Suspensory ligaments taut - pulls lens
Long thin lens
Little refraction to focus

173
Q

How do parasympathetic nerves control accommodation of the eye?

A

CLOSE VISION: stimulates parasympathetic nerves

Stimulation of oculomotor nerve (3) → Ach release → acts on M3 receptors → contracts smooth muscle cells →
Ciliary muscle contracted causes
Ciliary bodies moving inwards/forwards so
Suspensory ligaments relaxed
Bulged lens shape →
Increased refraction to focus

174
Q

How can drugs affect accommodation of the eye?

A

Both Muscarinic agonists and antagonists can cause blurred vision

175
Q

Bladder voiding involves interactions with…

A

Parasympathetic, sympathetic, motor and sensory afferent nerves

176
Q

Brainstem micturition centre

A

Coordinates bladder reflex to cause voiding

177
Q

Where are pre ganglionic sympathetic nerves found?

A

Lumbar region of spinal cord

178
Q

SNS in bladder voiding

A

Pre ganglionic SNS fibres get info from micturition centre -> send info via pre and post ganglionic fibres to bladder and innervate:

  1. Muscle wall (detrusor muscle - smooth muscle cells)
  2. Internal sphincter

Release Noradrenaline to act on B2 receptors on detrusor muscle to cause relaxation, expanding bladder enabling bladder to fill more

NA also at A1 receptors at internal sphincter constricting smooth muscle to ‘close the tap’ so no leaky bladder

179
Q

PNS in bladder voiding

A

Parasympathetic pre ganglionic fibres in Sacral region of spinal cord - receive info from micturition centre and send info via pre and post ganglionic fibres to detrusor muscle of bladder

→ Release Ach acting on M3 receptors of smooth muscle cells in bladder wall → contraction

Increases pressure and helps eject urine from bladder

180
Q

Motor nerves in bladder voiding

A

Motor nerves travel to smooth muscle cells of external sphincter of bladder, act at nicotinic receptors to contract (hold) or relax (void)

Motor nerves travel from sacral region of spinal cord

181
Q

Mechano-sensitive afferent fibres and bladder voiding

A

Sensory nerves (mechanoreceptors) found in wall of smooth muscle of bladder wall, sense when bladder is full

Stimulated when bladder is full → send info to micturition centre that bladder is full

182
Q

Process of bladder voiding through innervation

A

When bladder full- SNS innervation = relaxation of wall + contraction of internal sphincter
Stimulates sensory nerves = send info to micturition centre to switch off SNS, turn on PNS → M3 receptors in bladder wall contract
So internal sphincter opens bc SNS gone and detrusor muscle wall contracts = increased pressure and tap open so able to void
Motor system allows external sphincter to relax in order to void

183
Q

Muscarinic activist effect on detrusor muscle

A

Mus agonists, e.g. Bethanechol – urinary incontinence due to detrusor neuropathy

Helps bladder to void in cases where PNS innervation may not be able to work (incontinence bc without contraction of detrusor muscle person can’t void)

184
Q

Muscarinic antagonist effect on detrusor muscle

A

Mus antagonists, e.g. oxybutynin – urinary incontinence due to over activity bladder

Overactive bladder, too much stimulation so bladder doesn’t fill properly and always wants to void so block M3 receptors to slow down this frequency

185
Q

What PNS nerve innervates GI tract?

A

Vagus nerve

186
Q

What receptors do parasympathetic nerves act on in the GI tract?

A

M3 receptors

187
Q

Parasympathetic innervation of GI tract

A

Stimulation of vagus nerve releases Ach which acts on M3 receptors
↓
Contraction of circular and longitudinal smooth muscle in GI tract
↓
Increased motility

Vagus also contains afferent (sensory) fibres – peristaltic reflex control

188
Q

GI tract secretions: Salivary gland innervation

A

Salivary glands- VII (facial) & IX (glossopharyngeal)

Stimulate acinar cells
↑ Amylase / mucins

189
Q

GI tract secretions: Gastric glands

A

Gastric glands - X (vagus)

Stimulate parietal cells
↑ Gastric acid

190
Q

GI tract secretions: Pancreatic glands

A

Pancreatic glands - X (vagus)

Stimulate acinar + islet cells
↑ Pancreatic secretions, e.g. insulin

191
Q

Side effects of Muscarinic antagonists that treat GI tract

A

Mus antagonists, e.g. Hyoscine (Buscopan) – treat IBS-like symptoms
May cause tachycardia, blurred vision etc

192
Q

Stimulation of what receptors contracts bronchi m=smooth muscle cells?

A

Stimulation of M3 receptors contracts bronchi smooth muscle cells causing bronchoconstriction

Parasympathetic innervation

193
Q

Why are ipratropium and tiotropium used as bronchodilators?

A

Stimulation of M3 receptors contracts bronchi smooth muscle cells causing bronchoconstriction- need to reduce this aka reduce M3 stimulation to increase airflow

Thus,

anti-muscarinic drugs are used as bronchodilators, e.g.

Ipratropium
Tiotropium

Used in COPD (chronic obstructive pulmonary disease)
Need to increase airway flow

194
Q

Problems with muscarinic antagonists in patients with bladder outflow problems?

A

In patients with bladder outflow problems and glaucoma
Mus antagonist will reduce urine outflow, increase intraocular pressure
Conditions also associated with elderly (as is COPD)
These are potential contraindications

195
Q

How does stimulation of M3 receptors lead to contraction of smooth muscle cells?

A

IN SM CELL:

Ach binds to M3
M3 is GPCR → Gq pathway stimulated
→ activates phospholipase C 
= PIP2 broken down into DAG + IP3
→ IP3 water soluble so moves to cytoplasm → binds to IP3R on sarcoplasmic reticulum → opens ligand gated calcium channels (IP3 MEDIATED CALCIUM RELEASE)
= rise of calcium in cell

(meanwhile DAG → activates protein kinase C → acts on ion channels to increase membrane excitability = depolarisation)
Depolarisation = activation of voltage gated calcium channels → calcium enters cell
= rise in calcium in cell

So now rise in calcium
→ Calcium calmodulin
→ myosin light chain kinase 
→ myosin light chain- phosphorylated
→ actin-myosin interactions = contraction
196
Q

PNS innervation of male genitalia

A

Specialised sacral parasympathetic ‘vasodilator’ nerves
innervate erectile tissue

Stimulation of these nerves release nitric oxide (NO) NOT Ach
Remember this is an exception to the normal rule

NO is a lipophilic, membrane-permeable gas

NO causes relaxation of vascular smooth muscle cells
composing the corpus cavernosum

Corpus cavernosum dilates and fills with blood

Produces and maintains erection

197
Q

Sildenafil (viagra)

A

Sildenafil (Viagra) - erectile-dysfunction, prevents breakdown of the actions of NO – increasing it vasodilator effects

198
Q

Stimulation of parasympathetic nerves leads to a reduction in heart rate. What best describes the receptor subtype involved?

A

M2 receptor

199
Q

A new anti-histamine drug is being designed to treat hay fever. Clinical trials indicate that the drug produces side effects of blurred vision, constipation, and tachycardia. What most likely describes the off target actions of this drug?

A

Muscarinic antagonist

remember M2 receptors in heart slow down HR

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