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OS 213: Pulmo (Exam 1) > Cough & Mucus Hypersecretion > Flashcards

Cough & Mucus Hypersecretion Flashcards

1
Q

What is cough?

A

A forced expulsive maneuver, usually against a closed glottis and which is associated with a characteristic sound

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2
Q

Where is the distinctive sound of cough from?

A

Explosive release of trapped and pressurized intrathoracic air from the sudden opening of the vocal folds

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3
Q

What makes cough “normal”?

A

It is an innate protective reflex serving a normal physiologic function

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4
Q

Cough is a critical element in the self-clearing mechanism of the lungs. What substances does it remove?

A

mucus, noxious substances, debris, foreign objects and infections from the pulmonary tract

(note: coughing helps protect lungs against aspiration)

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5
Q

Enumerate the impact of cough

A
  • Can be harmful and deleterious if persistent and excessive
  • Common symptom for which patients seek medical attention
  • Discomfort from cough and other complications
  • Associated with marked deterioration in QoL, interferes with normal lifestyle

(note: psychosocial dysfunction returns to normal with successful treatment)

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6
Q

Most sensitive sites for initiating cough?

A

larynx & tracheobronchial tree (especially carina and branching points)

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7
Q

Afferent nerve endings richly innervate the __, __, and __ to the level of the terminal bronchioles and extend into the lung parenchyma.

A

pharynx, larynx, airways

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8
Q

Cough starts with…?

A

irritation of cough receptors

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9
Q

Phases of mechanism of cough: 2.5 L of air is inspired in this phase

A

Inspiratory phase - vocal cords open widely to let additional air into lungs
- negative flow rate

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10
Q

Phases of mechanism of cough: pressure in lungs rise to as high as 300 mmHg; markedly positive pressure causes narrowing of trachea

A

Compression phase - zero flow rate

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11
Q

Phases of mechanism of cough: air expelled at velocities ranging from 120 to
160 kph; shearing force s that develop aid in the elimination of mucus and foreign materials

A

Expulsion phase - 1st cough sound, positive flow rates

note: opening of vocal cords before sound

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12
Q

Phases of mechanism of cough: restorative inspiration

A

Recovery phase

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13
Q

Flow & subglottic pressures during cough phases: identify if subglottic pressure is negative, increasing, decreasing

Inspiratory (negative flow rate): ___
Compression (zero flow rate): ___
Expulsion (positive flow rate): ___

A

Inspiratory: negative
Compression: increasing
Expulsion: decreasing

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14
Q

What causes the noncartilaginous part of intrathoracic trachea to invaginate when coughing?

A

forced expiratory effort

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15
Q

Effect of tracheal narrowing during a cough?

A

Air rushing with a high linear velocity through the exceedingly narrow trachea dislodges the material to be dispelled and propels it into the throat

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16
Q

Normal values of normal trachea vs narrowed trachea:

Intrathoracic pressure (cm H2O): -4 vs __
Cross-sectional area (cm^2): 1.5 vs __
Volume flow, L/sec: 1 vs __
Linear velocity , cm/sec: 667 vs __

A

+ 150
0.25
7
28,000

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17
Q

Why is glottic closure not critical to effective coughing?

A

You can still have the coughing maneuver to expel things lodged in the airway even without this phase (e.g. patient under mechanical ventiliation or tracheostomy)

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18
Q

Cough reflex: how is cough initiated? Cite 4 reasons

A

1) Inflammatory or mechanical changes in the airways
2) Inhalation of chemical and mechanical irritants: polymodal sensory nerve receptors
3) Rapid and large changes in lung volumes
4) Psychological factors, e.g., laughter

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19
Q

Cough sensor plasticity is the exaggerated response to harmless or mildly irritating stimuli. What can lead to this?

A

Prolonged exposure to such irritants may initiate airway inflammation, which can itself precipitate cough and sensitize the airway to other irritants

(irritants can be endogenous or exogenous)

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20
Q

Peripheral mechanism of cough: Key Receptors and Ion Channels in
the Afferent Cough Reflex

Enumerate the channels that are involved in C fibre chemosensors (4) and the A-delta fibre mechanosensors (1)

A

C fibre: P2X3, TRPM8 (transient receptor potential melastin 8 ), TRPA1 (- transient receptor potential ankyrin 1), TRPV1 (transient receptor potential vanilloid 1)

A-delta: ASIC (acid sensing ion channels)

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21
Q

C fibers and A-delta fibers are the main vagal afferents mediating cough. C-fiber cell bodies are located in the ___, while Alpha-delta fibers are in the ___.

A

C fibers: superior vagal (jugular) ganglion, terminating in the paratrigeminal nucleus
Alpha-delta: e inferior vagal (nodose) ganglion, terminating in the nucleus of the solitary tract

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22
Q

Part of brain responsible for reflex coughing & voluntary cough/urge to cough:

A

reflex- respiratory CPG (central pattern generator)
voluntary- higher level cognitive, motor, and sensory processing

(note: full spectrum of cough)

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23
Q

Key Ion Channels in the Afferent Cough Reflex

This potential, with sufficient magnitude, stimulate the opening of voltage-gated sodium channels, leading to action potentials and sensory nerve activation.

A

Generator potential - membrane depolarization, induced by the opening of specific ion channels expressed by the terminals of vagal sensory nerves

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24
Q

Key Ion Channels in the Afferent Cough Reflex

The majority of chemical mediators that evoke generator potentials act via ____ receptors (give examples.

A

ionotropic receptors s (e.g., transient receptor potential vanilloid-1 (TRPV1) and P2X receptors)

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25
Q

This can activate P2X3 channels (recall: what type of vagal afferent is it assoicated with?)

A

ATP - pass through pannexin channels, lead to depolarization

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26
Q

SARS-CoV-2 might induce cough via _____ and _____ mechanisms.

A

neuroinflammatory & neuroimmune

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27
Q

Proposed Mechanism of Cough in SARS-COV2 Infection

Direct infection/viral recognition by (what type of neurons?) or (what type of glial cells?) could promote a (neuroinflammatory? or neuroimmune?) state, characterized by (what neuronal or glial activity characterizes the former state?)

A

vagal sensory neurons
neuron-associated glial cells
neuroinflammatory state
neuronal or glial release of neuroactive inflammatory mediators

28
Q

Proposed Mechanism of Cough in SARS-COV2 Infection

At what levels can neuroinflammation occur? (4)

A

nerve terminal in the airways and lungs
within the vagus nerve containing the neuronal axons
at the level of the vagal sensory ganglia containing neuronal cell bodies
at sites within the CNS responsible for integrating vagal sensory inputs

29
Q

Proposed Mechanism of Cough in SARS-COV2 Infection

Neuroinflammatory mediators which are important for antiviral responses within the nervous system?

A

neuronally released interferons and glial-derived ATP

30
Q

Proposed Mechanism of Cough in SARS-COV2 Infection

Identify if traditional inflammatory cell or if inflammatory mediator (released by traditional cells involved in SARS-CoV-2 infection)

macrophages
ATP
antiviral interferons
dendritic cells 
lipid mediators
prostanoids
neutrophils
cytokines
epithelial cells
A 
macrophages (T)
ATP (IM)
antiviral interferons (IM)
dendritic cells (T)
lipid mediators (IM)
prostanoids (IM)
neutrophils (T)
cytokines (IM)
epithelial cells (T)

Many of these mediators can activate or sensitise vagal sensory nerves via cognate receptors or gating ion channels, providing a neuroimmune axis for alterations in vagal sensory neuron activity

31
Q

Proposed Mechanism of Cough in SARS-COV2 Infection

Sensory neuron activation could enhance inflammation via the release of _____, which facilitate inflammatory cell ______ and ______ in a process known as ________

A

neuropeptides
recruitment & activation
neurogenic inflammation

32
Q

Proposed Mechanism of Cough in SARS-COV2 Infection

Receptors/channels involved in neuro-immune modulation (4)

A

IFNAR=interferon receptor
P2X2/3=purinergic receptors
TNFR=tumour necrosis factor receptor
TRPs=transient receptor potential channels

(note: TLRs=toll-like receptorsare involved in neuroinflammation with ACE2=angiotensin-converting enzyme 2)

33
Q

Pathophysiology of chronic cough: excessive coughing in disease is a consequence of repetitive activation of the neuronal pathways mediating cough. What are the two broad mechanisms via which they may occur?

A

1) increased exposure of the sensory nerve terminals to chemical irritants (e.g. PGE2, ATP) or excess mucus
2) changes in excitability of the neuronal pathways that may affect airway sensory nerves and/or their central nervous system connections

34
Q

The Cough Reflex: Signalling Pathways in The Development of Cough (see diagram, 39th slide)

1) location of cough receptors (5)
2) Identify the effector of each efferent nerve
spinal motor -
phrenic -
vagus -

A

1) larynx and supralaryngeal area, trachea and bronchi, ear canal and eardrum, pleura + pericardium + diaphragm, esophagus and stomach
2) spinal motor - expiratory muscles (including pelvic sphincters), phrenic - diaphragm, vagus - larynx, trachea, bronchi

35
Q

Fluid which protects the airways, constituting a physical barrier and a
medium with antimicrobial and immunomodulatory properties

A

airway lining fluid

(note: Lungs are exposed daily to 10,000 to 12,000 L of inhaled air, which potentially carries pathogens and noxious particles)

36
Q

Mucus is continuously produced and swept by ciliary action in what direction?

A

from distal to proximal conducting airways (mucus is swallowed after passing through larynx)

37
Q

Two layers of mucus:

A

gel (mobile mucus layer) & sol (periciliary layer of higher osmotic modulus)

38
Q

What gives the periciliary/sol layer its high osmotic modulus?

A

glycocalyx containing glycosaminoglycans, membrane-tethered mucins, and other glycoconjugates

39
Q

Composition of normal mucus and how much produced in a day

A 
95% water
3% mucin
1% lipids 
< 0.3% DNA
• Others: electrolytes, enzymes, oxidants, anti-oxidants, mediators, bacterial products, antibacterial secretions

20-30 mL in 24h

40
Q

Mucin confers
Liquid-like property that resist flow: ___
Solid-like capacity to store energy that moves or deforms the fluid: ___

A

viscosity (stickiness)

elasticity (stringiness)

41
Q

Promoting Mucociliary Clearance and Cough

Identify if it favors mucociliary clearance or cough:

Direct relationship with viscosity
Thick mucus layer
"Ideal" sol depth
Indirect relationship with elasticity
Direct relationship with elasticity
Thin mucus layer
Excess sol (heigh above cilia)
Indirect relationship with viscosity
A

Direct relationship with viscosity (cough)
Thick mucus layer (cough)
“Ideal” sol depth (MC)
Indirect relationship with elasticity (cough)
Direct relationship with elasticity (MC)
Thin mucus layer (MC)
Excess sol (heigh above cilia) (cough)
Indirect relationship with viscosity (MC)

42
Q

MUCIN

identify the number
__ human MUC genes
__ expressed in the human respiratory tract
__ classic gel-forming mucins found in airway secretion

A
43
Q

Enumerate the 3 gel-forming mucins found in airway secretions (which one is produced at proximal airways by goblet cells? which one is produced by goblet cells throughout the airway and by submucosal glands?)

Enumerate membrane-tethered mucins (3)

A

MUC2, MUC5AC (proximal), MUC5B (submucosal glands)

MUC1, MUC4, MUC16

44
Q

Define mucin: Complex glycoproteins; (rich in what?) secretory mucins stabilized by (what bonds?) -> (??) in a mesh

A

cysteine-rich
multiple disulphide bonds (S-S)
entangled

45
Q

About MUC5B:
Is it produced constitutively by surface epithelium?
Is it produced at the more proximal airways? If not, where?

Compare MUC5B with MUC5AC

A

MUC5B is produced constitutively by surface epithelium down to the level of bronchioles proximal to terminal bronchioles, and by submucosal glands present in the trachea and bronchi but not bronchioles. MUC5AC is
produced constitutively by surface epithelial cells with a goblet morphology in more proximal airways, and its production can be induced in non-goblet secretory cells that produce MUC5B down to the level of terminal bronchioles.

46
Q

Sequelae of increased mucous production (6)

A
  • Viscosity of mucus
  • ↓ Ciliary effectiveness
  • Mucus plugs
  • Airway Resistance
  • Infections
  • Atelectasis (d/t obstructed bronchioles)
47
Q

Factors Contributing to Cough Inefficiency/ Impaired Cough

Identify if altered cough mechanics or altered mucous rheology
adhesiveness
expiratory muscle weakness
inspiratory muscle weakness
cohesiveness
abdominal wall muscle weakness
A

Altered cough mechanics

a. Expiratory muscle weakness
b. Inspiratory muscle weakness
c. Abdominal wall muscle weakness
2. Altered mucous rheology
a. Adhesiveness
b. Cohesiveness
3. Altered mucociliary function

48
Q

Etiology of cough?

A

Any disorder resulting in inflammation, constriction, infiltration or compression of the upper or lower airways and the lung parenchyma can be associated with cough

49
Q

Assessment of Cough:

1) Resonance of the cough, its time of occurrence during the day, and the
pattern of coughing (e.g., occurring in paroxysms) frequently provide useful
etiologic clues: true or false?
2) What are useful historical questions? Give 3.
3) Give 3 instances where cough worsens
4) ENT/GI examination should be included in assessment: true or false?
5) Clues that could suggest cardiopulmonary disease? (2)
6) What can general examination rule out?

A

Except for our ability to detect the sound of excess airway secretions, details as to the resonance of the cough, its time of occurrence during the day, and the pattern of coughing (e.g., occurring in paroxysms) infrequently provide useful etiologic clues.
• Regardless of cause, cough often worsens upon first lying down at night, with
talking, or with the hyperpnea of exercise; it frequently improves with sleep.
• An exception may involve the cough that occurs only with certain allergic
exposures or exercise in cold air, as in asthma.
• Useful historical questions include what circumstances surrounded the onset of cough, what makes the cough better or worse, and does the cough produce
sputum.
• The physical examination seeks clues suggesting the presence of cardiopulmonary disease, including findings such as wheezing or crackles on
chest examination.
• Assessment should also include a thorough ENT/GI examination
• General examination is likewise important (e.g., clubbing, rashes) to rule out
cough as a manifestation of a systemic disisase such as sarcoidosis, vasculitis or cancer

50
Q

How to differentiate acute, sub-acute, and chronic cough?

A

acute: < 3 weeks
sub-acute: 3-8 weeks
chronic: > 8 weeks (can be a disease in itself, not just a symptom)

51
Q

Laboratory work-up of cough

What can the chest radiograph identify?

A

presence of chest wall, pleural, lung parenchymal and mediastinal lesions or abnormalities

52
Q

Laboratory work up of cough

SPUTUM ANALYSIS - gross and microscopic examination

1) What does purulent sputum indicate?
2) What to rule out when there is blood in the sputum?
3) What to do next when pneumonia or lung abscess is present?
4) When to use GeneXpert?
5) What does eosinophlia indicate?

A

1) chronic bronchitis, bronchiectasis
2) rule out endobronchial tumor
3) do G/S, C/S
4) GeneXpert (formerly, AFB smears): initial lab recommended for a Filipino with >2wks cough, esp. if with constitutional Sx’s
5) asthma or nonasthmatic eosinophilic bronchitis (NAEB)

53
Q

Approach to Acute Cough in Adults (also see diagram in ppt)

1) Etiology of acute cough (3)
2) Most common cause
3) What can happen when there is viral infection of the respiratory epithelium?
4) Which is though to be the major mechanism causing cough in acute bronchitis: excessive mucus production or hypersensitivity of afferent sensory nerves?

A
  • Acute cough is often due to a respiratory tract infection, aspiration, or inhalation of noxious chemicals or smoke.
  • Most common cause: Common Cold/ URTI/ acute bronchitis – 90% due to virus (50%, rhinovirus): antibiotics NOT needed
  • Viral infections of the respiratory epithelium cause early release of many inflammatory mediators disrupting the respiratory epithelium, sensitising chemosensitive cough receptors and the neuronal pathway of the cough reflex.
  • Hypersensitivity of the afferent sensory nerves is thought to be the major mechanism causing cough in acute bronchitis, not the production of excessive mucus.
54
Q

Approach to sub-acute cough in adults (study diagram as well)

1) A common residuum of tracheobronchitis - (what are the other two names?), resulting from (what are the causes?) following viral infection, pertussis, or infection with (what organisms/pathogens?)
2) If post-infectious, what to consider?
3) How to manage of not post-infectious in nature?
4) Lingering effects of an exacerbation of a preexisting condition: true or false?

A

1) A common residuum of tracheobronchitis - “postviral tussive syndrome“ or “postinfectious cough”, resulting from persistent airway inflammation and/or postnasal drip following viral infection, pertussis, or infection with Mycoplasma or Chlamydia
2) Post-Infectious Cough with BHR; Atypical causes of RTI/ pneumonia including Pertussis, PTB, atypical pneumonia, parasitic infections
3) Evaluated and managed as if it were chronic cough
4) True

55
Q

Evaluation and Treatment of Chronic Cough

What are the four steps?

A

Exclude & treat obvious cause(e.g., ACEI, cancers, inhaled foreign bodies)

Investigate/ treat common triggers (asthma, GERD, UACS); consider PTB in the Philippines

Make sure you are not missing rarer triggers

Control / suppress cough for Refractory or Unexplained Chronic Cough & CHS

56
Q

Description of patients with Cough Hypersensitivity Syndrome (2)

Epidemiology of patients with CHS (2)

A

Description: exquisite sensitivity to inhalation of environmental irritants & heightened sensitivity of the neuronal pathways mediating cough

epid: 2/3 females, peak at 50s-60s

57
Q

Characteristics of CHS (3; define them)

A
  • Hypertussivity: cough is triggered by normally subthreshold amounts of known cough-evoking agents
  • Allotussivity: cough is triggered by stimuli that do not usually cause cough in healthy individuals
  • Independent of etiology of cough
58
Q

Complications of cough

1) chest and abdomen?
2) can syncope occur?
3) fractures where?
4) complications related to QoL (4)
5) tracheobronchial complication?
6) another complication in the chest?
7) complication related to ENT?

A

1) chest and abdominal wall soreness
3) yes cough syncope can occur
3) rib fractures
4) exhaustion, insomnia, lifestyle change, urinary incontinence
5) tracheobroncial trauma
6) pneumothorax
7) hoarseness

59
Q

What is specific or targeted cough therapy?

A

Treat underlying cause

eliminate the inciting agent whenever possible

60
Q

Identify if antitussive/cough suppressant or protussive )non-specific cough therapy when cough performs no useful function/causes marked discomfort or sleep disturbance)

  • drugs that increase the latency or threshold of the cough center, e.g., codeine, dextromethorphan
  • enhance cough effectiveness by promoting the clearance of airway secretions and loosen mucus
  • pharmacologic agents, e.g., nebulized saline solution, erdosteine
  • for irritative, nonproductive cough
  • drugs that affect the afferent limb of the cough reflex, e.g., levodropropizine
  • indicated in cystic fibrosis, bronchiectasis, pneumonia and postoperative atelectasis
  • centrally acting neurokinin1 (NK-1) receptor antagonists, e.g., aprepitant for lung cancer
A

A - drugs that increase the latency or threshold of the cough center, e.g., codeine, dextromethorphan
P - enhance cough effectiveness by promoting the clearance of airway secretions and loosen mucus
P - pharmacologic agents, e.g., nebulized saline solution, erdosteine
A - for irritative, nonproductive cough
A - drugs that affect the afferent limb of the cough reflex, e.g., levodropropizine
P - indicated in cystic fibrosis, bronchiectasis, pneumonia and postoperative atelectasis
A - centrally acting neurokinin1 (NK-1) receptor antagonists, e.g., aprepitant for lung cancer

Protussive: a cough productive of significant quantities of sputum should usually not be suppressed, since retention of sputum in the tracheobronchial tree may interfere with the distribution of alveolar ventilation and the ability of the lung to resist infection

61
Q

Airway Secretion Management: Mucoactive Agents

1) How to increase sol layer?
2) Used to alter consistency of gel layer?
3) Used to improve ciliary activity?

A

1) water, saline, expectorants
2) mucolytics
3) corticosteroids, sympathetic bronchodilators

62
Q

Identify the specific disorder:

Previously known as “post-nasal drip syndrome”
Mechanism: secretions from nose/sinuses stimulate upper airway cough receptors; inflammation increases receptor sensitivity

A

Upper Airway Cough Syndrome

63
Q

Identify the specific disorder:

Eosinophilic airway inflammation WITHOUT variable airflow obstruction or airway hyperresponsiveness

A

Non-Asthmatic Eosinophilic Bronchitis (NAEB)

64
Q

Identify the specific disorder:

Likely due to extensive inflammation and disruption of upper and/or lower airway epithelial integrity
Often associated with the accumulation of an excessive amount of mucus hypersecretion and/or transient airway and cough receptor
hyperresponsiveness
Self-limiting

A

Post-infectious cough

65
Q

Identify the specific disorder:

Accumulation of protussive mediators such as bradykinins and substance P in the resp. tract with ACEI; bradykinins stimulate production of prostaglandins

A

ACE-induced cough

66
Q

Identify the disorder (review them!)

1) episodic/intermittent cough, with identifiable triggers, accompanied by dyspnea, chest tightness or wheezing, improves with bronchodilators, has Hx of childhood asthma and/or atopy, family Hx of asthma/ atopy
2) “tickle” in throat; throat clearing, hoarseness, nasal congestion/ discharge, postnasal drip, nasal obstruction, sneezing
3) Signs: inflamed nasal mucosa, secretions in posterior oropharynx, cobbledstone appearance of posterior pharynx
4) Cough that has been present for at least 3 weeks following a flu-like illness, not more than 8 weeks
5) dry cough, scratchy throat, feeling of throat obstruction
6) heartburn, regurgitation, ‘acidic’ taste, dysphagia, epigastric pain, hoarseness, sore throat, throat clearing; Worsens when lying supine
7) Cough usually resolves within 1 to 4 weeks of cessation, up to 3 months (mean: 26 d)

A

1) cough variant asthma
2) UACS
3) UACS
4) post-infectious cough
5) ACEI-induced cough
6) GERD/LPR/reflux-cough syndrome
7) ACEI-induced cough

OS 213: Pulmo (Exam 1) (2 decks)

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