MP324- COUGHING AND BREATHING PROBLEMS Flashcards
what happens with a cough
- deep inspiration followed by a build up of intra-thoracic pressure against a closed glottis
- glottis open and rapid expulsion of air and sound
500MPH
causes of dry cough
asthma
cold
GERD
sleep apnea
vocal cord dysfunction
allergies
COVID
causes of wet cough
cold
flu
lung infection
cystic fibrosis
COPD
acute bronchitis
bronchiectasis
easing coughs originating above the larynx
often helped by meds which form a soothing coat over the inflamed membranous tissue
(DEMULCENT)
easing coughs originating below the larynx
- eased by steam inhalation or water aerosol inhalations
- menthol, eucalyptus and benzoin tincture can help stimulate the secretion of a thin layer of mucus to protect the inflamed area
- menthol can block TRPV1 channels
- cough mixtures
suppression of a cough centrally
- opioids can suppress neuronal activity in the medulla
- codeine and methadone: activates u-opioid receptors (help lung cancer) with pain relief and better sleep (sedation)
- dectromethorphan and pholcodeine: act via mu-opioid receptors and are anti-tussive without pain relief
ATP as a key modulator of the cough reflex
- tussive stimuli from various various sources can increase calcium efflux, leading to ATP release from the open pannexin-1 channel
- ATP stimulates the P2X3 and P2X2 receptors on sensory neurones within the airway mucosa
- promising antitussive efficacy of P2X3 antagonists
the problem with mucus
- during infection or illness, more mucus produced and glycoproteins in the mucus can change (MORE VISCOUS)
- in bronchiectasis and CF mucus is very viscous and not easily cleared
- COPD mucus plugs - no airflow below part of lungs
mucolytics
N-acetylcysteine (NAC)
carbocysteine
dornase-a
solution to excessive mucus
MUCO-ACTIVE DRUGS
- mucolytics
- expectorants encourage productive cough by stimulating secretion of mucus (more watery)
- Muco-kinetic drugs, cilia beat faster
- Muco-regulators
Dornase-a MOA
- mucolytic enzyme
- used in CF
- can break down DNA polymers found in the thickened mucus and make it less viscous
expectorant example
guaifenesin
mucolytics MOA
break apart the di-sulphide bonds in the mucins, this decreases the viscosity of mucus
muco-kinetic drug examples
beta-2 adrenergic agonists
Muco-regulator drugs examples
anti-muscarinics
glucocorticoids
surfactants MOA
produced from type II pneumocystis and lower surface tension on the alveolar surface - reduced inner pressure within the alveoli
what happens without surfactant
the small alveoli would collapse and gas exchange would be severely compromised
also prevents so much fluid coming from the capillaries into the lungs (sealant)
Infant respiratory distress syndrome
- occurs in 50% of neonates between 26-28 weeks but becomes less frequent with development
- alveoli collapse leaving larger spaces that get filled with cellular debris
- layer of dead cells, proteins and surfactant on the surface of the alveoli
- gaseous exchange is severely compromised
symptoms of infant respiratory distress syndrome
breathing difficulties
blue colouration of the baby
apnoea
treatment options for infant respiratory distress syndrome
- pre-treatment of the mother with glucocorticoids can enhance surfactant secretion
- 40% oxygen, mechanical ventilation, fluids and artificial surfactants are used for symptoms
apnoea vs dyspnoea
apnoea -> stopping breathing
dyspnoea -> difficulty breathing
2 types of apnoea
obstructive
Central
obstructive apnoea
collapsible airways
narrow airways
central apnoea
neurological misfunction/imbalance
no inspiration
apnoea
- sleep apnoea common in babies
- prolonged apnoea can impair brain oxygenation
- avoiding sleeping on back, hypnotic drugs, alcohol and respiratory depressants (heroin)
type I respiratory failure
- low level of oxygen in the blood (hypoxemia)
- associated with damage to the lung tissue which prevents adequate oxygenation of the blood however the remaining normal lung is still sufficient to excrete carbon dioxide
- low oxygen PO2 <60mmHg but normal or lower PCO2
HIGH O2 THERAPY 85-95%
type II respiratory failure
- alveolar ventilation is insufficient to excrete the carbon dioxide being produced
- high PCO2 (hypercapnia)
- respiratory acidosis
low O2 therapy (24-28%)
