MP324- COUGHING AND BREATHING PROBLEMS Flashcards

1
Q

what happens with a cough

A
  • 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

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2
Q

causes of dry cough

A

asthma
cold
GERD
sleep apnea
vocal cord dysfunction
allergies
COVID

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3
Q

causes of wet cough

A

cold
flu
lung infection
cystic fibrosis
COPD
acute bronchitis
bronchiectasis

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4
Q

easing coughs originating above the larynx

A

often helped by meds which form a soothing coat over the inflamed membranous tissue
(DEMULCENT)

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5
Q

easing coughs originating below the larynx

A
  • 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
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6
Q

suppression of a cough centrally

A
  • 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
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7
Q

ATP as a key modulator of the cough reflex

A
  • 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
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8
Q

the problem with mucus

A
  • 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
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9
Q

mucolytics

A

N-acetylcysteine (NAC)
carbocysteine
dornase-a

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10
Q

solution to excessive mucus

A

MUCO-ACTIVE DRUGS
- mucolytics
- expectorants encourage productive cough by stimulating secretion of mucus (more watery)
- Muco-kinetic drugs, cilia beat faster
- Muco-regulators

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11
Q

Dornase-a MOA

A
  • mucolytic enzyme
  • used in CF
  • can break down DNA polymers found in the thickened mucus and make it less viscous
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12
Q

expectorant example

A

guaifenesin

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13
Q

mucolytics MOA

A

break apart the di-sulphide bonds in the mucins, this decreases the viscosity of mucus

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14
Q

muco-kinetic drug examples

A

beta-2 adrenergic agonists

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15
Q

Muco-regulator drugs examples

A

anti-muscarinics
glucocorticoids

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16
Q

surfactants MOA

A

produced from type II pneumocystis and lower surface tension on the alveolar surface - reduced inner pressure within the alveoli

17
Q

what happens without surfactant

A

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)

18
Q

Infant respiratory distress syndrome

A
  • 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
19
Q

symptoms of infant respiratory distress syndrome

A

breathing difficulties
blue colouration of the baby
apnoea

20
Q

treatment options for infant respiratory distress syndrome

A
  • pre-treatment of the mother with glucocorticoids can enhance surfactant secretion
  • 40% oxygen, mechanical ventilation, fluids and artificial surfactants are used for symptoms
21
Q

apnoea vs dyspnoea

A

apnoea -> stopping breathing
dyspnoea -> difficulty breathing

22
Q

2 types of apnoea

A

obstructive
Central

23
Q

obstructive apnoea

A

collapsible airways
narrow airways

24
Q

central apnoea

A

neurological misfunction/imbalance
no inspiration

25
Q

apnoea

A
  • sleep apnoea common in babies
  • prolonged apnoea can impair brain oxygenation
  • avoiding sleeping on back, hypnotic drugs, alcohol and respiratory depressants (heroin)
26
Q

type I respiratory failure

A
  • 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%

27
Q

type II respiratory failure

A
  • alveolar ventilation is insufficient to excrete the carbon dioxide being produced
  • high PCO2 (hypercapnia)
  • respiratory acidosis

low O2 therapy (24-28%)