9 Sensory Aspects of Respiratory Disease Flashcards

1
Q

Q: Define symptom. 3 examples related to respiratory disease.

A
A: 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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2
Q

Q: Define physical sign. 4 examples related to respiratory disease.

A

A: 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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3
Q

Q: What are the 2 parts leading to a conscious sensation? Pathway (5,3). Variation.

A

A: 1. sensory stimulus (e.g. pain from a cut in the skin) -> transducer (sensor) -> excitation of sensory nerve -> (afferent nerves lead to CNS) integration of CNS -> CNS creates a sensory impression = NEUROPHYSIOLOGY

  1. (sensory impression) -> perception (of information) -> (brain interprets the information coming from the sensory nerves and you get) evoked sensation = BEHAVIOURAL PSYCHOLOGY (eg removal of hand from hot plate)

People react differently to different sensations

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4
Q

Q: Why is a cough considered crucial? (2) Second to? but important when?

A

A: crucial defence mechanism protecting the lower respiratory tract from

     i) inhaled foreign material 
     i) excessive mucous secretion

Usually secondary to mucociliary clearance- BUT important in lung disease when mucociliary function is impaired and mucous production is increased

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5
Q

Q: Name a phase of a cough and state what occurs. What facilitates this? (2)

A

A: Expulsive phase of cough

generates a high velocity of airflow facilitated by bronchoconstriction and mucous secretion

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6
Q

Q: Describe nerve profiles in airways. (3)

A

A: - lots of nerve terminals project out into airway from rich plexus of fibres

  • well placed to sense the external environment (e.g. by mechanical stimulation of the nerve terminal by dust or right next to goblet cell)
  • nerve terminal could respond by triggering a cough
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7
Q

Q: What are the 3 types of stretch receptors in the airways and lungs?

A

A: 1. C – fibre receptors (fibres particularly sensitive to chemicals)

  1. Rapidly adapting stretch receptors (to a stimulus)
  2. Slowly adapting stretch receptors
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8
Q

Q: What are C-fibre receptors? (2) Where are they found? (4) What do they react to? (2) What do they release? (3)

A

A: “free” nerve endings of small unmyelinated fibres (C)
Larynx, trachea, bronchi, lungs

  • Chemical irritant stimuli
  • inflammatory mediators

Release neuropeptide inflammatory mediator:

  • Substance P
  • Neurokinin A
  • Calcitonin Gene Related peptide
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9
Q

Q: What are rapidly adapting stretch receptors? Where are they found? (4) What do they respond to? (3)

A

A: Small, myelinated nerve fibres (A delta)

  • naso-pharynx
  • larynx
  • trachea
  • bronchi
  • Mechanical= mainly to inflammation (increased tracheal pressure)
  • chemical irritant stimuli
  • inflammatory mediators
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10
Q

Q: What are slowly adapting stretch receptors? Where are they found? (2) act as? What do they respond to?

A

A: Myelinated nerve fibres

Located in airways smooth muscle- Predominantly in trachea and main bronchi

Mechanoreceptors -> Respond to lung inflation/inflammation (increased tracheal pressure)

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11
Q

Q: Recording from airway vagal afferent nerves in an experiment using anaesthetised rats.

Why vagal afferent nerves?
What is given as a stimulus?
How do C-fibres respond to the stimulus?
How do rapidly acting and slow adapting stretch receptors react to the stimulus?
What is the next stimulus? why?
How do rapidly acting and slow adapting stretch receptors react to the stimulus?

A

The vagus is the 10th Cranial Nerve through which ALL sensory nerves from the airways pass through to the brain

Caspaicin has been given which is a stimulus to the sensory nerves

C: stimulated when the caspaicin is injected intravenously

no effect on them

tracheal pressure (MAIN STIMULUS for the rapidly and slow adapting stretch receptors is INFLATION)

rapidly adapting stretch receptors STOP firing + slow adapting stretch receptors are STIMULATED to fire

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12
Q

Q: What are the 2 main receptors to the cough reflex? What’s the difference? What do they each respond to? (2,4)

A

A: Mechanorsensors (only myelinated stretch receptors) and Nociceptors (stretch or C fibre)

M have cell bodies in nodose ganglion
N have cell bodies in jugular ganglion

MECHANOSENSORS are activated by:

  • Mechanical Displacement
  • CITRIC ACID

NOCICEPTORS are activated by:

  • CASPAICIN
  • Bradykinin
  • Citric Acid
  • Cinnamaldehyde
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13
Q

Q: Name 3 things that are present on nociceptors? Shape of mechanosensors?

A

A: TRPV1, TRPA1 and B2

bit like a tree

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14
Q

Q: Describe the afferent pathway for a cough. (5)

A

A: 1. Mechanical
(e.g. dust, mucous, food/drink)

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

  1. stimulation of irritant receptors (RARs)/cough receptor which are mechanical or chemical
  2. go via vagus nerve (or superior laryngeal nerve if from pharynx/larynx) up brainstem
  3. to ‘cough centre’ in medulla
  4. to cerebral cortex
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15
Q

Q: Describe the efferent pathway for a cough. (3)

A

A: 1. cerebral cortex of brain has analysed info coming in

  1. to ‘cough centre’ in medulla
  2. stimulation of various muscles leading to the and the production of sound
    i) closure of the glottis
    ii) expiratory muscles of abdomen
    iii) diaphragm
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16
Q

Q: What are the 3 phases of a cough? Draw a graph. What’s brain activity like when you feel like you need to cough? Sound?

A

A: 1. Inspiratory Phase = opens up the trachea

  1. Glottic Closure (main sound starts at end of this)
  2. Expiratory Phase

REFER- subglottic pressure (below larynx) and flow rate lines

brain is really active when you feel the need to cough eg premotor cortex

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17
Q

Q: How does pressure change during the act of a cough? What does this do? result? contributes to?

A

A: increase in intrapulmonary pressure

compresses the posterior membrane of the trachea which pushes through and narrows the trachea into a crescent shape

increases flow and contributes to the sound produced (as air is pushed through narrowing)

18
Q

Q: Cough sound waveforms. Describe. (How many phases? How many sounds?)

A

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

19
Q

Q: What happens to give someone a whooping cough?

A

A: tracheal collapse during cough

20
Q

Q: Name non respiratory diseases that cause a cough. (3) Drug?

A

A: -mid ear pathology

  • CVS disease eg LV failure
  • obstructive sleep apnoea

angiotensin-converting E inhibitor medications (eg for heart failure)

21
Q

Q: What is the most common type of cough? cause? Symptoms (4). How long does it last?

A

A: acute cough (<3wks)

Common cold from rhinovirus

Cough
Post nasal drip
Throat clearing
Nasal blockage

22
Q

Q: What cough lasts longer than an acute cough? What could be the cause? (5)

A

A: Chronic persistent cough (> 3 weeks)

Asthma and eosinophilic-associated (25%)
Gastro-oesophageal reflux (25%)
Rhinosinusitis (associated with postnasal drip) (20%)
Chronic bronchitis (‘smoker’s cough) (8%)
Drugs eg Angiotensin converting enzyme inhibitor (1%)

23
Q

Q: How can phlegm vary?

A

A: if discoloured, can show infection

24
Q

Q: Describe a chronic cough. Cause? Control? What can trigger it? (7)

A

A: increased cough reflex = ‘Cough Hypersensitivity Syndrome’

Irritation in the throat or upper chest

Cough paroxysms difficult to control (not throat clearing)

  • Deep breath, laughing, talking too much,
  • vigorous exercise;
  • Smells (perfumes, vinegar)
  • Cigarette smoke
  • Eating crumbles (biscuits)
  • Cold air
  • Lying flat
25
Q

Q: How can we measure hypersensitivity in the lung (cough)? What do we use? How do results differ with non chronic coughers and chronic coughers?

A

A: use caspaicin from chillies

activates TRPV1 receptor on nociceptors

for a normal none cougher- as you inhale increasing amounts of caspaicin-> doesn’t start coughing straight away-> coughs at solution 6

for a chronic cougher- start coughing at first solution or even before

26
Q

Q: What mechanism gives you hypersensitivity in terms of a cough? Describe 3 examples.

A

A: Plasticity of neural mechanisms (changing their sensitivity)

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

27
Q

Q: Management of cough hypersensitivity syndrome as sensory neuropathic cough. 2 methods. (4,4)

A

A: Speech pathology management

  • to increase voluntary control
  • to decrease cough sensitivity
  • to decrease laryngeal irritation
  • to decrease laryngeal muscle contraction

Pharmacology (use to suppress cough eg if cause is unknown)

  • Amitryptiline
  • Gabapentin
  • Opiates: morphine, codeine, dextrometorphan
  • Experimental: TRPV1 blockers
28
Q

Q: Name the sensory inputs for pain fibres from the following structures:

Nose
Pharynx
Larynx
Lungs
Chest wall
A
A: Nose = Trigeminal (V)
Pharynx = Glossopharyngeal (IX) Vagus (X)
Larynx = Vagus (X)
Lungs = Vagus (X)
Chest wall = spinal nerves
29
Q

Q: Why do we need to distinguish between touch and pain? (2) Similarity?

A

A: anatomical pathways are slightly different, as are the sensory receptors

Both touch and pain information goes to the primary somatosensory cortex

30
Q

Q: Touch anatomical pathway. Travels via which fibres and where? Where do they go? (3) Example.

A

A: Touch travels via A alpha and A beta fibres via the dorsal horn

TOUCH - goes to the contralateral side at the level of the caudal medulla (brainstem)

  • > thalamus
  • > primary somatosensory cortex

EXAMPLE: the sensation of touch from the leg will run up along the same side as the leg it is coming from and then cross onto the other side at the brainstem

31
Q

Q: Pain anatomical pathway. Travels via which fibres and where? Where do they go? (3) Example.

A

A: travels via A delta and C fibres via dorsal horn and then spino thalamic tract

PAIN - goes to the contralateral side at the same anatomical level (it crosses right away)

  • > thalamus
  • > primary somatosensory cortex
32
Q

Q: What is the main difference between the pain and touch pathways? What’s the clinical importance? Explain.

A

A: The MAIN DIFFERENCE between the two pathways is really at the level at which the pathways cross through to the contralateral side (pain crosses straight away at lower spinal level end while touch in medulla)

Brown-Sequard Syndrome (hemisection of the spinal cord= cutting the spinal cord in half on one or the other side)

If you have hemisection on the LEFT SIDE of the spinal cord, the touch sensation will be fine on the opposite side but the pain sensation on the other side will be affected

33
Q

Q: What are the 2 types of pain? Where do they arise? How do the number of afferents differ? Which one is difficult to localise? what can this lead to?

A

A: Visceral pain (from visceral organs eg heart, gi tract, bronchial wall) is not the same as somatic pain (from skin)

Number of visceral afferents is less than number of somatic afferents

Visceral pain is difficult to localise, diffuse in character and is referred to somatic structures

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.

34
Q

Q: Chest pain from respiratory system. 4 causes. Examples (4,2,4,1)

A

A: Pleuropulmonary disorders:

  • Pleural inflammation from infection
  • pulmonary embolism,
  • Pneumothorax
  • malignancy eg mesothelioma (cancer of pleura)

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 eg pain down left arm that we know comes from heart attack

35
Q

Q: Causes of chest pain not from respiratory disorders. 3 types and examples (2,3,1).

A

A: Cardiovascular disorders

  • Myocardial ischaemia/infarction
  • Pericarditis

Gastrointestinal disorders

  • Oesophageal rupture
  • Gastrooesophageal reflux
  • Pancreatitis

‘Psychiatric disorders’
-panic disorder

36
Q

Q: Activation related to graded pain intensity Somatosensory processing. Name 5 areas.

A

A: 1. Primary & secondary somatosensory cortex
Posterior insular cortex

  1. Motor processing (since you want to remove your arm from hot water)
    Cerebellum, putamen, ventral premotor cortex
  2. Affective processing:
    Anterior cingulate cortex, insular cortex
  3. Attentional processing:
    Anterior cingulate cortex,
    primary somatosensory cortex,
    Ventral premotor cortex
  4. Autonomic function (you react to pain eg cry)
    Anterior cingulate cortex, anterior insular cortex
37
Q

Q: What is dysponea? When does it occur (how do you judge how severe it is)? (2) What type of experience is it? What is associated with it? How can if affect life?

A

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 (difficult to gauge how bad it is yourself) and) dyspnea may be life-threatening

38
Q

Q: How can you grade dysponea? (2)

A

A: Clinical dyspnea scale (American Thoracic Society) = looks at how much work you have to do before you get breathless (0 to 10)

Modified Borg scale (very descriptive intensity of sensation)

39
Q

Q: Name and describe 3 respiratory descriptors.

A

A: air hunger cluster= hunger for more air/ urge to breathe more

work/effort cluster= breathing requires effort

tightness cluster= heaviness/tightness on/in chest

40
Q

Q: How do you assess shortness of breath/dysponea? (4)

A

A: 1. Volunteered comments & clinicians’ assessment

  1. Subjective rating scales
    Visual analogue
    Modified Borg
  2. Questionnaires
    i) Exercise tolerance related (Eg. Baseline Dyspnea Index, Shortness of Breath Questionnaire)
    ii) Quality of life (Eg. SF36, St George’s Respiratory Questionnaire)
  3. Exercise testing
    6 minute walk test
    Shuttle test
41
Q

Q: Name some orders that present with dysponea/ chronic SoB. (5)

A

A: Impaired pulmonary function

  • Airflow obstruction eg Asthma, COPD,
  • Extrathoracic pulmonary restriction eg pleural effusion
  • Neuromuscular weakness eg Phrenic nerve paralysis

Impaired cardiovascular function

  • Myocardial disease leading to heart failure
  • Congenital vascular disease

Altered central ventilatory drive or perception

  • Metabolic acidosis
  • Anaemia

Physiologic processes eg hypoxic high altitude, pregnancy

Idiopathic hyperventilation

42
Q

Q: How do you treat dysponea? (6)

A

A: 1. Treat the cause (eg lung or cardiac)
2. Treatment of dyspnea itself is difficult

Therapeutic options:

  1. Add bronchodilators eg b-adrenergic agonists
  2. Drugs affecting brain eg morphine, diazepam
  3. Lung resection (eg lung volume reduction surgery)
  4. Pulmonary rehabilitation (improve general fitness, general health, psychological well-being)