Sensory aspects of respiratory disease Flashcards

1
Q

Outline the prevalence of different respiratory symptoms

A
Cough
Third most common complaint heard by GP
10-38% of patients in respiratory outpatients complain of cough
Chest pain
Most common pain for which patient seeks medical attention (35%), including acute chest pain
Shortness of breath (SOB, dyspnea)
6-27% of general population
3% of visits to A&E
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2
Q

What is meant by symptoms of respiratory disease

A
SYMPTOMS
An abnormal or worrying sensation that leads the 
person to seek medical attention
e.g.   Cough
         Chest pain
         Shortness of breath
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3
Q

What is meant by a physical sign of respiratory disease

A

PHYSICAL SIGN
An observable feature on physical examination
e.g. Hyperinflation of chest wall
Dullness on percussion of chest wall
Increased respiratory rate
Reduced movement of chest wall

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4
Q

Describe conscious sensation production

A
  1. The sensory stimulation (e.g. a cut) activates sensory transducers which transmit the signal via excitation of sensory nerves (afferent nerves into the CNS).
  2. CNS creates a sensory impression – neurophysiology.
    a. This impression leads to the perception of information.
  3. The brain interprets the information coming from sensory nerves and evokes a ‘sensation’ – behavioural psychology.
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5
Q

Describe the function of cough

A

A crucial defence mechanism protecting the lower respiratory tract from
inhaled foreign material
excessive mucous secretion
Usually secondary to mucociliary clearance
but important in lung disease when mucociliary function is impaired and mucous production is increased

Mucous reaches large airways- then you cough

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6
Q

Describe the expulsive phase of coughing

A

Inhaled material and material brought up the broncho-pulmonary tree to the trachea and larynx by mucocilliray clearance can trigger a cough reflex
This is caused by a reflex deep inspiration that increases intrathoracic pressure whilst the larynx is closed
The larynx is suddenly opened, producing a high-velocity jet of air, which ejects unwanted material at a high speed through the mouth
facilitated by bronchoconstriction and mucous secretion.

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7
Q

Describe the nerve profile in the airways

A
• Image	
 on	
 the	
 left	
 shows	
 a	
 nerve	
 terminal	
 on	
 the	
 surface	
 of	
 the	
 epithelium	
 	
  • It	
 is	
 well	
 placed	
 to	
 sense	
 the	
 external	
 environment	
 (e.g.	
 by	
 mechanical	
  stimulation	
 of	
 the	
 nerve	
 terminal	
 by	
 dust)	
 	
  • This	
 nerve	
 terminal	
 could	
 respond	
 by	
 triggering	
 a	
 cough

Some on goblet cells- sensitive to mucus

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8
Q

Summarise the localisation of cough receptors

A

Rapidly adapting irritant receptors which are located within airway epithelium.
Most numerous on posterior wall of trachea,
At main carina, and branching points of large airways, less numerous in more distal airways. Absent beyond the respiratory bronchioles.
Also in the pharynx. Possibly also in the external auditory meatus, eardrums, paranasal sinuses, pharynx, diaphragm, pleura, pericardium, and stomach.
Stimuli: laryngeal and tracheobronchial receptors respond to chemical and mechanical stimuli.

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9
Q

Describe the different nerves involved

A

Vagus- stomach, trachea, bronchi, ear drums
Trigemminal- para nasal sinuses
Glossopharyngeal- larynx

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10
Q

Describe the different types of nerve fibres

A
§ Slow adapting stretch receptors. 
o Main stimulus is inflation. 
§ Rapidly adapting stretch receptors. 
o Main stimulus is inflation. 
§ C-fibre receptors. 
o Main stimulator is chemicals like capsaicin.
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11
Q

Describe C-fibres

A

C – fibre receptors
“free” nerve endings
Larynx, trachea, bronchi, lungs
Small unmyelinated fibres (C)
Chemical irritant stimuli, inflammatory mediators
Release neuropeptide inflammatory mediators Substance P, Neurokinin A, Calcitonin Gene Related peptide

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12
Q

Describe rapidly adapting stretch receptors

A

Rapidly adapting stretch receptors
Naso-pharynx, larynx, trachea, bronchi
Small, myelinated nerve fibres (A)
Mechanical, chemical irritant stimuli, inflammatory mediators

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13
Q

Describe slowly adapting stretch receptors

A
Slowly adapting stretch receptors
Located in airways smooth muscle
Myelinated nerve fibres
Predominantly in trachea and main bronchi
Mechanoreceptors
Respond to lung inflation
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14
Q

What do all the sensory nerves in the airways pass through to reach the brain

A

ALL sensory nerves from the airway pass through the 10th cranial nerve, AKA the Vagus nerve.

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15
Q

Describe the experiments which demonstrated the functions of the different nerve fibres

A
• The	
 above	
 image	
 shows	
 measurements	
 of	
 the	
 action	
 potential,	
 tracheal	
  pressure	
 (P)	
 and	
 arterial	
 blood	
 pressure	
 (ABP)	
  • Caspaicin	
 has	
 been	
 given	
 which	
 is	
 a	
 stimulus	
 to	
 the	
 sensory	
 nerves	
 	
  • C-­‐fibres	
 are	
 stimulated	
 by	
 CHEMICALS	
  • The	
 C-­‐fibre	
 is	
 stimulated	
 when	
 the	
 caspaicin	
 is	
 injected	
 intravenously	
 	
  • The	
 caspaicin	
 has	
 NO	
 EFFECT	
 on	
 the	
 rapidly	
 and	
 slow	
 adapting	
 stretch	
  receptors	
 	
  • The	
 MAIN	
 STIMULUS	
 for	
 the	
 rapidly	
 and	
 slow	
 adapting	
 stretch	
 receptors	
 is	
  INFLATION	
  • INCREASE	
 in	
 tracheal	
 pressure	
 =	
 rapidly	
 adapting	
 stretch	
 receptors	
 STOP	
 firing	
  \+	
 slow	
 adapting	
 stretch	
 receptors	
 are	
 STIMULATED	
 to	
 fire	
 	
  • These	
 receptors	
 are	
 most	
 likely	
 to	
 be	
 involved	
 in	
 coughin
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16
Q

Distinguish between the stimuli for rapidly and slow adapting stretch receptors

A
o Hyperinflation (mechanical) stimulates a rapid response.
o Hyperinflation (mechanical) stimulates a slow response.
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17
Q

Describe mechanoreceptors

A

o Activated by mechanical displacement and citric acid.
o Look like a tree.

Transmit vagus nerve afferents through nodose ganglion via myelinated A alpha fibres

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18
Q

Describe noicireceptors

A

o Activated by capsaicin, bradykinin, citric acid and cinnamaldehyde.
o TRPV1, TRPA1 and B2 channels are present.

Transmit vagus nerve afferents via unmyelinatec C-fibres through nodose ganglion

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19
Q

List some receptors involved in sensing mechanical and chemical changes

A

TRPV1: Transient receptor potential vanniloid-1 receptor
TRPA1: Transient receptor potential cation channel, subfamily A1
ASIC: Acid-sensing ion channel
B2: Bradykinin receptor B2

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20
Q

Describe the afferent neural pathways for cough

A
Stimulation of
irritant receptors (RARs)/
Or cough receptor
Mechanical
(e.g. dust, mucous, food/drink)

Chemical
(e.g. noxious, intrinsic inflammatory agents)

stimulation of irritant receptors leads to firing down Vagus nerve to cough centre in medulla- superior laryngeal nerve joins from larynx

Some also sent to other parts of the cerebral cortex

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21
Q

Describe the efferent neural pathways for cough

A

Cerebral cortex communicates with medullary cough centre

Efferents sent to glottis (to close it)
Diaphragm, external intercostals and the accessory muscles of inspiration

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22
Q

Summarise the full neural pathway for cough

A
• Sensory	
 information	
 goes	
 via	
 the	
 vagus	
 nerve	
 and	
 through	
 the	
 brainstem	
 to	
  the	
 cough	
 centre	
  • The	
 cough	
 centre	
 consists	
 of	
 the	
 nucleus	
 tractus	
 solitarius	
 -­‐	
 a	
 collection	
 of	
  neurons	
 that	
 are	
 connected	
 to	
 the	
 medullary	
 cough	
 pattern	
 generator	
  • The	
 reflex	
 is	
 probably	
 a	
 brainstem	
 reflex	
 
Laz’s	
 Notes	
 	
  Respiratory	
 	
 	
  108	
  • From	
 the	
 medullary	
 cough	
 pattern	
 generator	
 you	
 get	
 stimulation	
 of	
 various	
  muscles	
 needed	
 to	
 produce	
 the	
 cough	
 	
  • The	
 complete	
 cough	
 pathways	
 also	
 includes	
 the	
 cerebral	
 cortex	
  • When	
 you	
 go	
 to	
 SLEEP,	
 this	
 reflex	
 is	
 INHIBITED	
 so	
 you	
 need	
 to	
 be	
 awake	
 to	
 a	
  certain	
 extent	
 to	
 be	
 able	
 to	
 cough	
 	
  • Under	
 general	
 anaesthetic	
 this	
 is	
 also	
 suppressed
23
Q

Outline the mechanics of coughing

A
• 	Inspiratory phase with negative flow during inhalation 
Glottic pressure in the minimum flow phase (glottis closes to generate pressure) 
Glottis opening 
Expiratory phase 
  • The	
 inspiratory	
 phase	
 opens	
 up	
  the	
 trachea	
  • During	
 the	
 act	
 of	
 coughing	
 there	
  is	
 an	
 increase	
 in	
 intrapulmonary	
  pressure	
 that	
 compresses	
 the	
  posterior	
 membrane	
 of	
 the	
  trachea	
 which	
 pushes	
 through	
  and	
 narrows	
 the	
 trachea	
 into	
 a	
  crescent	
 shape	
 	
  • This	
 increases	
 flow	
 and	
 contributes	
 to	
 the	
 sound	
 produced	
 	
  • NOTE:	
 the	
 brain	
 is	
 really	
 active	
 when	
 you	
 feel	
 the	
 need	
 to	
 cough	
 	
 
24
Q

Describe the cough sound waveforms

A

2 phases with an initial explosive phase that is the first cough sound, followed by an intermediate phase with decreasing sound.

an additional third phase called voiced or glottal phase which gives rise to a second cough sound.

25
Q

List some common causes of cough

A

§ Acute infection – e.g. bronchopneumonia, rhinovirus.
§ Chronic infection – e.g. CF or TB.
§ Airways disease – e.g. Asthma.
§ Parenchymal disease – e.g. Emphysema.
§ Tumours.
§ Foreign bodies.
§ Cardiovascular problems – e.g. Left ventricular failure.
§ Other disease – e.g. Recurrent aspiration, GERD.
§ Drugs – e.g. ACE inhibitors.

26
Q

List the common types of acute cough (< 3 weeks)

A
Common cold:
Cough
Post nasal drip
Throat clearing
Nasal blockage
Nasal discharge
Rhinovirus most common cause- symptoms disappear after 2 weeks
27
Q

List the causes of a chronic persistent cough

A
Asthma and eosinophilic-associated (25%)
Gastro-oesophageal reflux (25%)
Rhinosinusitis (postnasal drip) (20%)
Chronic bronchitis (‘smoker’s cough) (8%)
Bronchiectasis (5%)
Drugs eg Angiotensin converting enzyme inhibitor (1%)
Post-viral (3%)
‘Idiopathic’ (10%)
Other causes (3%)
28
Q

Describe Gastro-oesophageal reflux and cough: mechanisms

A

Oesophageal bronchial’ reflex (i)

 Direct action of protons on 
cough receptors (ii)

Activation of brain stem
‘cough’ centers (iii) in NTS- efferents to respiratory muscles and cough

29
Q

How does sputum change in infection

A

May become a yellowish or green colour

30
Q

Summarise cough hypersensitivity syndrome

A

Irritation in the throat or upper chest

Cough paroxysms difficult to control (not throat clearing)

Triggers: Deep breath, laughing, talking too much,
vigorous exercise;
Smells (perfumes, vinegar)
Cigarette smoke
Eating crumbles (biscuits)
Cold air, changing temperatures
Lying flat

31
Q

What is a chronic cough or cough hypersensitivity syndrome indicative of

A

Increased cough reflex

32
Q

How can you measure the sensitivity of the cough reflex

A
Sensitivity	
 of	
 the	
 cough	
 reflex	
 can	
 be	
 measured	
 using	
 caspaicin	
  o Caspaicin	
 is	
 the	
 thing	
 in	
 chilies	
 that	
 give	
 them	
 their	
 hotness	
 	
  o You	
 initially	
 give	
 a	
 dilute	
 solution	
 of	
 caspaicin	
 and	
 then	
 increase	
 the	
  concentration	
 until	
 the	
 participant	
 coughs	
 	
  o Chronic	
 coughers	
 are	
 particularly	
 sensitive	
 to	
 caspaicin	
  • Caspaicin	
 an	
 activate	
 nociceptors	
 through	
 TRPV1	
 receptors	
 
33
Q

Describe the plasticity of neural mechanisms

A

Excitability of afferent nerves increased by chemical mediators eg prostaglandin E2
Increase in receptor numbers eg TRPV-1 (transient receptor potential vanniloid-1 or capsaicin receptor), voltage-gated channels
Neurotransmitter increase eg neurokinins
in brain stem

34
Q

Describe TRPV-1

A
  1. Calcium-permeable, non-selective cation channel
  2. Activated by vanilloid ligands (eg capsaicin, endocannabinoid, noxious heat & H+); 12-lipoxygenase metabolites
  3. Expressed in sensory neurones of dorsal root and trigeminal ganglia

Expressed more in patients with a chronic cough

35
Q

Summarise the mechanism of chronic cough

A
• There	
 may	
 also	
 be	
 an	
 increase	
 in	
 inflammatory	
 mediators,	
 which	
 damage	
 or	
  change	
 the	
 reactivity	
 of	
 the	
 nerves	
 to	
 various	
 stimuli	
 like	
 caspaicin	
  • NOTE:	
 this	
 diagram	
 shows	
 that	
 smooth	
 muscle	
 hypertrophy	
 in	
 asthma	
 could	
  affect	
 the	
 slowly	
 adapting	
 receptors	
 that	
 could	
 contribute	
 to	
 enhanced	
  hypersensitivity	
 
36
Q

Describe symptomatic suppressive therapy

A

Central action:
Opiates: Codeine, dihydrocodeine, pholcodeine,
Dextromethorphan, (Morphine, diamorphine)
Peripheral action:
Moguistine, levodopropizine,

37
Q

Describe disease specific therapy

A

Eosinophil-associated: Inhaled corticosteroids
Gastro-oesophageal reflux disease: Proton pump inhibitors,
Histamine H2 antagonists
Post-nasal drip (rhinosinusitis): Topical steroids, antihistamines
Bronchiectasis: Postural drainage, Antibiotics

38
Q

Summarise the use of antitussives

A
• If	
 you	
 are	
 coughing	
 excessively	
 then	
 you	
 might	
 want	
 to	
 suppress	
 it	
 but	
 not	
  completely	
 eliminate	
 the	
 cough	
 response	
 because	
 then	
 you’d	
 be	
 getting	
 rid	
 of	
  its	
 defensive	
 capabilities	
  • Opiates	
 can	
 act	
 as	
 an	
 antitussive	
 but	
 they	
 are	
 not	
 particularly	
 effective	
 as	
 they	
  work	
 at	
 doses	
 where	
 there	
 are	
 a	
 lot	
 of	
 side-­‐effects	
 (e.g.	
 morphine	
 and	
 codeine)	
 
39
Q

Describe speech pathology management

A

↑voluntary control
↓ cough sensitivity
↓laryngeal irritation
↓laryngeal muscle contraction

40
Q

Outline the locations of the different inputs

A

Nose
Trigeminal (V)

Pharynx
Glossopharyngeal (IX) Vagus (X

Larynx
Vagus (X)

Lungs
Vagus (X)

Chest wall
spinal nerves

41
Q

Summarise the anatomical pathways of touch and pain

A

§ Touch and pain have slightly different pathways.
§ The main difference is at which level the pathways cross to the contra-lateral side:
o Touch – crosses at the caudal medulla.
o Pain – crosses at the same anatomical level, i.e. straight away.
§ Brown-Sequard Syndrome – hemisection of the left side of the spinal cord means touch will be fine but pain will be felt on the other side of the body.

As and Ab in touch pathway

Aalpha and C fibres in pain pathway

42
Q

Describe the different types of pain

A
Visceral pain (from visceral organs eg heart, gi tract, bronchial wall) is not the same as somatic pain (from skin). 
Visceral pain is difficult to localise, diffuse in character and is referred to somatic structures.
Number of visceral afferents is less than number of somatic afferents 
Pain arising from various viscera in the thoracic cavity and from the chest wall is often qualitatively similar and exhibits overlapping patterns of referral, localisation and quality, leading to difficulties in diagnosis.
43
Q

Describe chest pain from the respiratory system

A

Pleuropulmonary disorders:
Pleural inflammation eg infection, pulmonary embolism,
Pneumothorax, malignancy eg mesothelioma

Tracheobronchitis:
Infections, inhalation of irritants

Inflammation or trauma to chest wall:
Rib fracture, Muscle injury, Malignancy, Herpes zoster (intercostal
Nerve pain)

Referred pain: shoulder-tip pain of diaphragmatic irritation

44
Q

Describe the non-respiratory causes of chest pain

A
Cardiovascular disorders
Myocardial ischaemia/infarction
Pericarditis
Dissecting aneurysm
Aortic valve disease
Gastrointestinal disorders
Oesophageal rupture
Gastrooesophageal reflux
Cholecystitis
Pancreatitis

‘Psychiatric disorders’
panic disorder
Self-inflicted

45
Q

describe the brain regions involved in pain

A

Brain regions involved: somatosensory processing occurs in the primary somatosensory cortex (motor in the cerebellum, attentional in primary somatosensory and autonomic in the cingulate/insular cortexes)

46
Q

What is dyspnoea

A

Troublesome shortness of breath reported by a patient
Occurs at inappropriately low levels of exertion, and limits exercise tolerance
Unpleasant and frightening experience. Can be associated with feelings of impending suffocation
Poor perception of respiratory symptoms and dyspnea may be life-threatening

47
Q

What are the different scales for dyspnoea

A

see tables

48
Q

Describe descriptions related to air hunger

A
Hunger for more air
Urge to breathe more
Starved for air
Suffocation or smothering
Short of breath
Breaths feel too small
49
Q

Describe symptoms associated with work/effort

A
Breathing requires effort
Breathing requires work
Breathing is uncomfortable
Feels like heavy exercise
Size of breaths feel too large
50
Q

Describe symptoms associated with tightness

A

Tightness/constriction in chest

Heaviness in my chest

51
Q

Describe the different methods for assessing shortness of breath and dyspnoea

A
Volunteered comments &amp; clinicians’ assessment
Subjective rating scales
Visual analogue
Modified Borg 
Questionnaires
Exercise tolerance related
Eg. Baseline Dyspnea Index, Shortness of Breath Questionnaire
Quality of life
Eg. SF36, St George’s Respiratory Questionnaire
Exercise testing
6 minute walk test
Shuttle test
52
Q

List some disorders presenting with chronic SOB or dyspnoea

A

Impaired pulmonary function
Airflow obstruction eg Asthma, COPD, tracheal stenosis
Restriction of lung mechanics eg idiopathic pulmonary fibrosis
Extrathoracic pulmonary restriction eg Kyphoscoliosis, pleural effusion
Neuromuscular weakness eg Phrenic nerve paralysis
Gas exchange abnormalities eg Right to left shunts
Impaired cardiovascular function
Myocardial disease leading to heart failure
Valvular disease
Pericardial disease
Pulmonary vascular disease
Congenital vascular disease
Altered central ventilatory drive or perception
Systemic or metabolic disease
Metabolic acidosis
Anaemia
Physiologic processes eg deconditioning, hypoxic high altitude, pregnancy, severe exercise
Idiopathic hyperventilation

53
Q

Summarise the general treatment of dyspnoea

A

Treat the cause (eg lung or cardiac)
Treatment of dyspnea itself is difficult
Therapeutic options:
Add bronchodilators eg anticholinergics or b-adrenergic agonists
Drugs affecting brain eg morphine, diazepam
Lung resection (eg lung volume reduction surgery)
Pulmonary rehabilitation (improve general fitness, general health, psychological well-being)