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Cough and difficult in
breathing
Name:- Bokkisham
Durgadevi
Group:- Gm20_116
Cough Definition
it is a sudden and variable expiratory thrust
of air from the lungs through the air passages
associated with phonation, which
momentarily interrupts the physiological
pattern of breathing Without an effective
cough reflex, there is a risk of retaining
airway secretions and aspirated material
predisposing to infection, atelectasis, and
respiratory compromise
Rapid inspiration
Closure of the glottis 3. Contraction of
the abdominal and expiratory thoracic
muscles 4. Abrupt increase in pleural
and intrapulmonary pressures 5.
Opening of glottis and expulsion of
burst of air from mouth
Pathophysiology of cough
Cough reflex initiated by chemical/mechanical stimuli This is carried by the afferents
which are type c and type 1 fibers and innervate pharynx, larynx ,large airways ,
terminal bronchiole and lung parenchyma Afferents travel via vagus and superior
laryngeal nerve NTS in brain stem is the cough center Efferents travel via vagus,
phrenic, spinal motor nerves to the larynx, trachea, bronchi, diaphragm producing
cough
Cough receptors- rapid acting receptors (RAR), slow acting receptors (SAR), C fibers,
and other cough receptors are Mechanosensitive and chemosensitive. Impulses from
these receptors are all carried by the vagus nerve
. •The receptors have nerve terminals under or within the epithelium concentrated at
points of airway branching. •They are polymodal and respond to a wide variety of
chemical n mechanical irritants, & by many inflammatory n immunologic mediators
like histamine, bradykinin, PGs n substance-P.
There occurs increase in sensitivity of RARs n C-fibers by allergen challenge, viral
infections, cigarette smoke and a variety of inflammatory mediators. RARs can also
be sensitized by mucus in the airways, underlying smooth muscle contraction n
mucosal edema.
. Voluntarily a person is capable of suppressing the reflex cough for some time Cough
can also be voluntarily induces (motor and pre motor areas of brain) Neuro
transmitters involved in voluntary control of cough are seratonin, gaba, dopamine,
nmda(N-methyl-D-aspartate ) etc The central nervous pathways for cough show
interactions and plasticity
. Efforts should be made to identify the cause of cough A cough lasting than more
than 3 wks require a detailed evaluation Cough associated with or without sputum is
more important than the amount of sputum and the presence or absence of sputum
Acute(<3) weeks
Tracheobronchitis Bronchopneumonia
Viral pneumonia Acute-on-chronic
bronchitis Pertussis Pulmonary
embolism Foreign body aspiration
Sudden onset – bronchial asthma
,asthmatic bronchitis , whooping cough,
foreign body ,LVF with PE
Subacute(3-8 weeks)
trachiobronchitis , pertussis , post viral
tussive syndrome
Chronic >8 weeks
Upper airway cough syndrome • Asthma •
Gastro oesophageal reflux disorder • Post
viral cough • Chronic bronchitis •
Bronchiectasis, cystic fibrosis • Ace inhibitor
induced Cough • Environmental irritants.
Treatment
Topical administration of corticosteroid
drops in the head- down position is the best
treatment, often with the concomitant use of
antihistamines. severe symptoms- short
course of oral steroids, followed by topical
therapy. A topical anticholinergic spray to the
nose (such as ipratropium bromide).
Antibiotic therapy is necessary in the
presence of acute sinusitis involving bacterial
infection with the presence of mucopurulent
secretions that has persisted for at least 10
days.
Dyspenia
breathing is difficult, laboured or
uncomfortable subjective awareness of need
for increased respiratory effort ventilatory
demands > ventilatory capacity
Pathophysiology of
Dyspenia
Dyspnea results when there is an imbalance
between the perceived need to breathe and
the perceived ability to breathe. CO2 build
up and oxygen deprivation were the critical
factors that result in dyspnea. Elevation in
CO2 levels appear to stimulate dyspnea
more than do low oxygen levels
Family history
allergy, collagen vascular disease. Addiction
history– smoking history, cocaine, opiate
overdose .Exposure to indoor pollutants
Treatment history—radiation(radiation
pneumonitis developing 6 weeks to 6 months
after radiation) , drugs( amiodarone,
nitrofurantoin, busalfan, adenosine ,
anorexigens, etc ) .
Thank you

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Bokkisham Durgadevi ppt8.. gm20116 cough and breathing problem

  • 1. Cough and difficult in breathing Name:- Bokkisham Durgadevi Group:- Gm20_116
  • 2. Cough Definition it is a sudden and variable expiratory thrust of air from the lungs through the air passages associated with phonation, which momentarily interrupts the physiological pattern of breathing Without an effective cough reflex, there is a risk of retaining airway secretions and aspirated material predisposing to infection, atelectasis, and respiratory compromise
  • 3. Rapid inspiration Closure of the glottis 3. Contraction of the abdominal and expiratory thoracic muscles 4. Abrupt increase in pleural and intrapulmonary pressures 5. Opening of glottis and expulsion of burst of air from mouth
  • 4. Pathophysiology of cough Cough reflex initiated by chemical/mechanical stimuli This is carried by the afferents which are type c and type 1 fibers and innervate pharynx, larynx ,large airways , terminal bronchiole and lung parenchyma Afferents travel via vagus and superior laryngeal nerve NTS in brain stem is the cough center Efferents travel via vagus, phrenic, spinal motor nerves to the larynx, trachea, bronchi, diaphragm producing cough Cough receptors- rapid acting receptors (RAR), slow acting receptors (SAR), C fibers, and other cough receptors are Mechanosensitive and chemosensitive. Impulses from these receptors are all carried by the vagus nerve . •The receptors have nerve terminals under or within the epithelium concentrated at points of airway branching. •They are polymodal and respond to a wide variety of chemical n mechanical irritants, & by many inflammatory n immunologic mediators like histamine, bradykinin, PGs n substance-P. There occurs increase in sensitivity of RARs n C-fibers by allergen challenge, viral infections, cigarette smoke and a variety of inflammatory mediators. RARs can also be sensitized by mucus in the airways, underlying smooth muscle contraction n mucosal edema. . Voluntarily a person is capable of suppressing the reflex cough for some time Cough can also be voluntarily induces (motor and pre motor areas of brain) Neuro transmitters involved in voluntary control of cough are seratonin, gaba, dopamine, nmda(N-methyl-D-aspartate ) etc The central nervous pathways for cough show interactions and plasticity . Efforts should be made to identify the cause of cough A cough lasting than more than 3 wks require a detailed evaluation Cough associated with or without sputum is more important than the amount of sputum and the presence or absence of sputum
  • 5. Acute(<3) weeks Tracheobronchitis Bronchopneumonia Viral pneumonia Acute-on-chronic bronchitis Pertussis Pulmonary embolism Foreign body aspiration Sudden onset – bronchial asthma ,asthmatic bronchitis , whooping cough, foreign body ,LVF with PE
  • 6. Subacute(3-8 weeks) trachiobronchitis , pertussis , post viral tussive syndrome
  • 7. Chronic >8 weeks Upper airway cough syndrome • Asthma • Gastro oesophageal reflux disorder • Post viral cough • Chronic bronchitis • Bronchiectasis, cystic fibrosis • Ace inhibitor induced Cough • Environmental irritants.
  • 8. Treatment Topical administration of corticosteroid drops in the head- down position is the best treatment, often with the concomitant use of antihistamines. severe symptoms- short course of oral steroids, followed by topical therapy. A topical anticholinergic spray to the nose (such as ipratropium bromide). Antibiotic therapy is necessary in the presence of acute sinusitis involving bacterial infection with the presence of mucopurulent secretions that has persisted for at least 10 days.
  • 9. Dyspenia breathing is difficult, laboured or uncomfortable subjective awareness of need for increased respiratory effort ventilatory demands > ventilatory capacity
  • 10. Pathophysiology of Dyspenia Dyspnea results when there is an imbalance between the perceived need to breathe and the perceived ability to breathe. CO2 build up and oxygen deprivation were the critical factors that result in dyspnea. Elevation in CO2 levels appear to stimulate dyspnea more than do low oxygen levels
  • 11. Family history allergy, collagen vascular disease. Addiction history– smoking history, cocaine, opiate overdose .Exposure to indoor pollutants Treatment history—radiation(radiation pneumonitis developing 6 weeks to 6 months after radiation) , drugs( amiodarone, nitrofurantoin, busalfan, adenosine , anorexigens, etc ) .
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