Lecture 19 - cough and breathing problems Flashcards

1
Q

what happens with a cough?

A

Deep inspiration followed by build up of intra-thoracic pressure against a closed glottis.
Glottis open and you have rapid expulsion of air and the sound.
500mph!

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2
Q

what are common causes of persistent cough and what can it be associated/ induced by?

A

Asthma, rhinosinusitis (with post nasal drip) and oesophageal reflux (GERD) are common causes of persistent cough.
Persistent cough can also be associated with lung cancer and chronic infections like TB and bronchitis.
Persistent cough can also be caused by medication, such as ACE inhibitors used in heart failure. In this instance the problem can be resolved by switching to an angiotensin II blocker.

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3
Q

what are causes of dry cough?

A

asthma, cold, Gerd, sleep apnea, vocal cord dysfunction, allergies, covid

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4
Q

what are causes of wet cough?

A

cold, flu, lung infection, cystic fibrosis, copd, acute bronchitis, bronchiectasis

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5
Q

what are cough originating above the larynx treated with?

A

Honey, thick sugar based syrups (with or without a central cough suppressant) and lozenges are useful for this purpose. Useful for about 30 minutes or so.
Sometimes children tend to swallow lozenges so placing the sweet on a stick may work better.

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6
Q

what are coughs originating below the larynx treated with?

A

Coughs originating below the Larynx may be eased by steam inhalation or water aerosol inhalations.

Menthol, eucalyptus and benzoin tincture can help by stimulating the secretion of a thin layer of mucus to protect the inflamed area.

Menthol can block TRPV1 channels (could be mode of suppression?).

Cough mixtures can contain a whole range of active constituents

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7
Q

what surpresses the cough centre in medulla?

A

Opioids:
Codeine and methadone. Activates µ-opioid receptors. Methadone and diamorphine linctus is sometimes helpful to lung cancer patients – they can help with pain relief (analgesia) and better sleep (sedation).

Dextromethorphan (non-addictive) and pholcodeine act via -opioid receptors. They are anti-tussive without offering pain relief. Dextromethorphan is common in OTC cough medicines.

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8
Q

how is ATP a key modulator of the cough reflex?

A

Geofery Burnstock proposed that ATP and related nucleotides could be neurotransmitters co-released with noradrenaline, which subsequently acted on non-adrenergic and non-cholinergic nerves
Tussive stimuli from various sources can increase the calcium influx, leading to ATP release from the open pannexin-1 channel.
ATP activates the P2X3 and P2X2/3 receptors on sensory neurones within the airway mucosa
Promising antitussive efficacy of P2X3 antagonists

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9
Q

what re breathing problems and easing breathing process

A

Mucus and airway function
Surfactant

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10
Q

describe the mucus lining the airways

A

Water (98%) salts (1%) and mucin glycoproteins (0.5%)
Mucins glycoproteins- hydrophilic
Mucins when secreted polymerise in to chains and networks
Dilute mucus is a fluid, concentrated mucus like a solid
dilute=lubricant……solid = adhesive

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11
Q

whiter are he muco-active drugs?

A

Mucolytics include N-acetylcysteine (NAC) and carbocysteine break apart the di-sulphide bonds in the mucins. This decreases the viscosity of mucus.
Dornase α is an mucolytic enzyme used in patients suffering from Cystic Fibrosis. Dornase α can break down DNA polymers found in the thickened mucus and so make it less viscous.
Expectorants such as guaifenesin encourage productive cough by stimulating secretion of mucus (more watery overall). Easier to clear.
Muco-kinetic drugs (cilia beat faster)- beta 2 adrenoceptor agonists.
Muco-regulators- anti-muscarinics, glucocorticoids.

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12
Q

what is Importance of surfactant

A

Surfactants, produced from type II pneumocytes lower surface tension on the alveolar surface- reduced inner pressure within the alveoli (and equalizes pressure between big and small alveoli)

Without surfactants, the small alveoli would collapse and gas exchange would be severely compromised.

Also prevents so much fluid coming from the capillaries into the lungs-kind of sealant.

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13
Q

what is Infant Respiratory Distress syndrome?

A

IRDS occurs in 50% of neonates born between 26-28 weeks, but becomes less frequent as development progresses.
IRDS occurs soon after birth, is associated with breathing difficulties, blue colouration of the baby and extended periods of breathing cessation (apnoea).
Alveoli collapse leaving larger spaces that get filled with cellular debris. This Diffuse Alveolar Damage (DAD) - layer of dead cells, proteins and surfactant on the surface of the alveoli (so-called hyaline membranes).
Gaseous exchange is severely compromised.

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14
Q

what are treatment options for infant respiratory syndrome?

A

Pre-treatment of the mother before she gives birth with glucocorticoids can enhance surfactant secretion and prevent many cases.
Treatment with 40% oxygen therapy, mechanical ventilation, fluids and artificial surfactants are used to combat the symptoms.
Artificial surfactants for intratracheal application include: colfosceril palmitate, poractant-α and beractant

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15
Q

describe synthetic surfactants vs natural?

A

Lucinactant reduced significantly the incidence of RDS at 24 hours, compared with colfosceril.
No significant difference in comparison with beractant (33.3%).
Lucinactant reduced significantly RDS-related mortality rates by 14 days of life, compared with both colfosceril and beractant.

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16
Q

what is sleep apnoea?

A

Apnoea- elderly, obese, diabetic, allergic reactions
Two types – obstructive and central
Obstructive –collapsible airways, narrow airways.
Central – neurological misfunction/imbalance no inspiration.
Prolonged apnoea can impair brain oxygenation.
Avoiding sleeping on one’s back, hypnotic drugs, alcohol and respiratory depressants (heroine)

17
Q

describe problems that arise in the body from sleep apnoea

A

depression, diabetes, heart failure, high blood pressure, concentration and memory problems

18
Q

what are treatment options used respiratory stimulants?

A

Mandibular advancement devices (MADs). Also CPAP (continuous positive airway pressure) devices- flow holds the airways open
Respiratory stimulants (analeptics) such as doxapram (Carotid) and aminophylline (central effect on the NTS)
Acetazolamide – some emerging evidence for moderate benefit for central sleep apnoea
Aminophylline can also be used as a respiratory stimulant for preterm neonates.
Mechanical ventilators are favoured over respiratory stimulants in most clinical trauma situations
Irritant vapours (such as ammonia) can also be used to stimulate breathing, especially following fainting

19
Q

what are most cases of breathlessness caused by?

A

cardiovascular disease,
pulmonary disease, COPD, pulmonary hypertension, pulmonary embolism.
Interstitial lung disease
psychogenic dyspnoea (anxiety)
deconditioning/obesity
anaemia

20
Q

what are cardiovascular problems linked to dyspnoea?

A

Heart failure – backward and forward failure
Back failure increased pulmonary venous pressure and movement of fluid into the air spaces of the lungs (pulmonary oedema)
Forward failure – heart too weak to perfuse the lungs
Pulmonary hypertension- narrowing of the arteries going to the lungs- less perfusion and right sided heart failure
Pulmonary embolism – block of the vessels in lung

21
Q

what are treatments for cardiovascular diseases which are linked to causing dyspnoea?

A

Acute, significant pulmonary oedema will require oxygen
Heart failure - Diuretics (e.g. furosemide) help reduce the oedema and vasodilators.
Longer term ACE inhibitors are then used to reduce the load on the heart.

Embolism - acute pharmaceutical treatment includes oxygen, thrombolysis and anticoagulation.
Surgery

22
Q

what is type 1 repiratory failure caused by?

A

Type -1 respiratory failure-low level of oxygen in the blood (hypoxemia).
Associated with damage to lung tissue which prevents adequate oxygenation of the blood. However, the remaining normal lung is still sufficient to excrete carbon dioxide

23
Q

what conditions is there low oxygen PO2 but normal or lower PCO2 in and what is the treatment?

A

Pneumonia, Acute respiratory distress syndrome, Pulmonary fibrosis, Pulmonary hypertension.
low oxygen PO2 (less than 60mmHg) but normal or lower PCO2 (≤ 45-50 mmHg)
Treatment - High O2 therapy 85-95% (Maybe invasive)

24
Q

what is type II respiratory failure caused by, conditions present in, features and treatment options?

A

Alveolar ventilation is insufficient to excrete the carbon dioxide being produced. It affects the lung as a whole.
COPD, severe asthma, strong opioids.
Normal/low PO2 (or > 60mmHg) but high PCO2 (hypercapnia) (>50mmHg). Also respiratory acidosis (pH <7.35)
Treatment - Low concentration O2 therapy (24-28%) (Non-invasive)
Don’t use high oxygenation. In COPD O2 levels are more important for driving respiration. Risk hypercapnia and respiratory acidosis