respiratory pathology 1 Flashcards
examples of obstructive lung diseases
emphysema , asthma , chronic bronchitis
what are obstructive lung diseases
these are diseases that cause difficulty in air flow during expiration
common term for bronchitis and emphysema
chronic obstructive pulmonary disease
spirometry values for obstructive lung diseases
FEV1 reduced by a large extent
FVC is also reduced that is the final amount of air that is breathed out .
FEV-1 and FVC ratio
FEV1 is usually about 70-80% of FVC
Normal FEV1 is about 3.5 – 4 litres
Normal FVC is about 5 litres
Normal ratio FEV1 : FVC is 0.7 – 0.8
clinical tests for obstructive lung disease
PEFR
spirometry
summary of obstructive lung disease
There is AIRFLOW LIMITATION
Peak Expiratory Flow Rate (PEFR) is reduced
FEV1 is REDUCED
FVC may be reduced
FEV1 is less than 70% of FVC
bronchial asthma
Generally considered to be REVERSIBLE airways obstruction either spontaneously or as a result of medical intervention ( both can be treated by medication )
COPD aetiology
smoking
dust particles from occupation
atmospheric particles in the inhaled air might lead to development of COPD
effect of age
more prevalent in adults
risk factors for development , progression and morbidity in COPD
individual and social factors
general external environment
early life risk factors
noxious exposures
definition of chronic bronchitis clinically
cough productive of sputum most days in at least 3 consecutive months for 2 or more years
morphological changes in chronic bronchitis
both the small and the large airways will be affected .
changes in the small airways in chronic bronchitis
Goblet cells appear
Inflammation and fibrosis in long standing disease
the changes in the small airways are more pathological as the small airways are gaseous exchange sites
morphological changes in the large airways
Mucous gland hyperplasia
Goblet cell hyperplasia (increase in number )
Inflammation and fibrosis is a minor component
emphysema
destruction of the alveoli without fibrosis
which is an increase in the air spaces distal to the terminal bronchiole arising either from dilatation or from destruction of their walls and without obvious fibrosis.
forms of emphysema
centriacinar
panacinar
periacinar
scar
bullous emphysema
centriacinar emphysema
loss of alveoli tissue occurs in the middle bit of the acinus( the most common )
centriacinar emphysema
begins with bronchiolar dilatation then the alveolar tissue is lost
panacinar emphysema
at the base of the alveoli and there is much more destruction
bullous emphysema
has no physiological consequences
scar emphysema ( bullous )
just underneath the pleura
could be present in young people
pathogenesis of emphysema
smoking
lack of alpha -1 -antitrypsin
ageing
smoking and emphysema
there is alot of production of protease and less of antiprotease which is a protective mechanism against inflammatory cells .
therefore there is
alpha -1- antitrypsin deficiency causes emphysema
there is no production of antiproteases so there is destruction of the alveoli by the anti-inflammatory cells
features of COPD that are reversible
smooth muscle tone and inflammation will respond to pharmacological intervention
what happens to the alveoli in emphysema
there is the loss of the radial pull of the terminal alveoli which later on leads to the collapse of the alveoli during expiration
hypoxaemia in COPD
this is the state of leaving with less oxygen and more co2
Airway Obstruction on expiration
Alveolar Hypoventilation - there is less carbon dioxide being taken out
Reduced Respiratory Drive - the chemoreceptors are less sensitive to changes in hydrogen ion concentration
Shunt - Only during severe acute infective exacerbation
changes in the pulmonary vessels
there is physiological vasoconstriction( remember shunt )
all vessels may constrict if there is hypoxaemia.
pulmonary hypertension
normally pulmonary circulation is of low systolic pressure ; in pulmonary hypertension there is :
1.Pulmonary vasoconstriction
2.Pulmonary arterioles
3.muscle hypertrophy and intimal fibrosis
4.Loss of capillary bed
5.Secondary polycythaemia – increased blood viscosity
6.Bronchopulmonary arterial anastamoses
chronic ( hypoxic ) cor pulmonale
this is hypertrophy of the right ventricle which results from disease affecting the function and or the structure of the lung
what is asthma
an obstructive respiratory disease that has no reliable diagnostic test and is mostly symptom based and is reversible
what are the main symptoms of asthma
coughing , wheezing , running out of breath and response to certain asthma medication which makes asthma reversible
causes of asthma
-Host (genes) response to environment
-Physiology abnormal before symptoms (predisposition)
-Host response to exposure important
-It is a syndrome
what are the types of asthma syndromes
infant onset
childhood onset
adult onset
excertional asthma
occupational asthma
main causes of asthma
genetic predisposition which lead to primary epithelial abnormality in the skin /airway /gut while epigenetics alter the disease that is they are a trigger of the disease.
proof of causation in adults
breast -feeding
late weaning
allergens that are released post and ante- natal.
smoking
symptoms to look out for asthma in children
when there is genuine wheezing , cough and shortness of breath .
when there is a problem with the upper respiratory tract
when there is sucking in of ribs
when there is response to corticosteroids ( that is the symptoms are reversed )
guidelines for diagnosis asthma in children
measure the FeNO level in children with a history suggestive of asthma
performing objective tests that may help support a diagnosis of asthma
treatment of suspected asthma for under fives
most likely to have recurrent LRTI
treated with low dose of inhaled corticosteroids and a review is done later on.
conditions that can cause isolated cough
Bronchitis
Pertussis
Habitual cough
Foreign body
conditions that cause difficulty in breathing
Dysfunctional breathing
Vocal cord dysfunction
conditions which cause isolated sounds in breathing
Bronchitis
Laryngomalacia
Tracheomalacia
Snoring
what are the goals for the treatment for asthma in children
“minimal” symptoms during day and night
minimal need for reliever medication
no attacks (exacerbations)
no limitation of physical activity
what to use with attacks that happen more than 2 days a week .
blue inhaler
what to use when coughing and waking up more than once in a week
blue reliever inhaler
questions for measuring control of asthma
SANE
Short acting beta agonist/week
Absence school/nursery
Nocturnal symptoms/week
Exertional symptoms/week
tests required for children
no tests are recommended
treatment hierarchy for asthma
1.Are the patient’s symptoms fully/partly/not controlled?
2.Are they taking their treatment (correctly)?
3.Have they had an attack recently?
4.How often are they using their reliever treatment?
5.What is their current treatment level?
restarting ICS
start on low dose of ICS
Then review after 2 months with no routine test to monitor progress required
withdraw from medication for 2 months to monitor.
as required therapy and maintenance and reliever inhaled corticosteroid
they only work in adults and are advocated by GINA , no evidence in children
treatment of chronic asthma in children
start on low dose ICS
if symptoms are uncontrolled introduce MART ,
if MART is working but not very effectively increase dose, then refer to specialist
if MART therapy is not working then introduce low dose LTRA , add LABA
inhaled corticosteroids
very effective and very safe
examples of inhaled corticosteroids
beclomethasone budesonide 1
ultrafine beclomethasone 2.5
fluticasone diproprionate 2
fluticasone fuorate 5
effects of inhaled corticosteroids
1.height suppression by 1 cm
2.sometimes oral candidiasis
3.adrenocortical suppression caused by the increased use of exogenous steroids
long acting beta agonist
should be used with ICS and is a fixed dose only
( flutiform)
leukotriene receptor antagonist
montelukast , there is better adhere and there are granules for toddlers
side effects of leukotriene receptor antagonist
psychiatric side effects
comparison between the different medication for chronic asthma
laba , ics, tra
medication combination for chronic asthma that leads to increased FEV1
low or moderate ICS plus LABA
severe asthma
refer to specialist
chronic asthma treatment for under fives
ICS , LTRA , LABA
methods of asthma drug delivery in children
MDI or a spacer
dry powder device
breath actuated
practices that promote 100 % drug delivery
washing the spacer device
shake the spacer device between puffs
non medicinal management of asthma in children
stop tobacco exposure
what are the treatment options for chronic asthma in children
laba
ltra
ics
mild acute asthma treatment
SABA via spacer and prednisolone
medication for moderate acute asthma
SABA via a nebuliser and prednisolone
SABA and ipratropium via nebuliser and prednisolone
medication for severe acute asthma
IV salbutamol
IV aminophylline
IV magnesium (neb)
IV hydrocortisone
Intubate and ventilate
mode of intake of steroids in children with acute asthma
oral steroids
mode of intake for steroids in children with chronic asthma
inhaled steroids
presentation of asthma in adults
shortness of breath
wheezing
coughing
onset of asthma in adults
marked at the beginning and the end of the day
amount of people with asthma in the uk
5.4 million
pathophysiology of asthma
narrowing of the airways, inflammation of the airways, increased airway sensitivity
risk factors for asthma in adults
smoking during pregnancy
genetic basis of asthma disease in the family
genetic predisposition of atopic diseases such as asthma , eczema , rhinitis and hay fever .
maternal atopy has a greater chance of causing asthma than paternal influence
environmental exposure
examples of atopic diseases
hay fever
eczema
allergic rhinitis
asthma
effects of maternal smoking during pregnancy on child resp system
FEV 1 decreases
asthma probability increases
airway responsiveness
this leads to switching on genes that can result in atopy ( epigenetics )
how does occupation increase chance of cancer in adults
Isocyanates twin pack paints
Colophony welding solder flux
Laboratory animals rodent urinary proteins
Grains wheat proteins, grain mites
Enzymes subtilisin, amylase
Drugs antibiotics, salbutamol
Crustaceans prawns, crabs
diagnosis test for asthma in adults
measure Fe NO first followed by spirometry then bronchodilator reversibility if there is an obstruction form the spirometry
Symptoms of asthma
the symptoms are variable depending on the season and whether it is day or night and exposure to certain trigger.
wheezing
shortness of breath on different severity
tightness of chest
dry cough
occasional sputum
SYMPTOMS THAT ARE NOT PROBABLY ASTHMA
Finger clubbing, cervical lymphadenopathy
Stridor( wheeze on inspiration)
Asymmetrical expansion, dull percussion note (collapse/ effusion)
Crepitations-crackles that is (bronchiectasis, Cystic Fibrosis, ILD interstitial liver disease , LVF liver function test )
localised airway obstruction diseases
Tumour
Foreign body
investigations of asthma in adults
evidence of airflow obstruction where the FEV1 test is less than 70% or where there is reversibility and variability of airway flow ( however , the spirometry test results may come out as normal especially when the person is not under an asthma attack)
ruling out other obstructive lung diseases
1.spirometry - spirometry test less than 70%
2.PEFR test is done to rule out COPD and emphysema
3.carbon monoxide gas transfer ( tlco for gas transfer and kco for tissue destruction)
4.use of bronchodilator for example inhaled salbutamol then nebulised salbutamol
5.reversibility with the use of oral corticosteroids which separates COPD form asthma
assessment of acute asthma
Ability to speak
Heart rate
Respiratory rate
PEF
Oxygen saturation / Arterial blood gases
moderate asthma
Able to speak, complete sentences
HR < 110
RR < 25
PEF 50 - 75% predicted or best
SaO2 ≥ 92% (no need for ABG)
PaO2 ≥ 8kPa
severe asthma
Inability to complete sentences in one breath
HR ≥110
RR ≥25
PEF 33 - 50% predicted or best
SaO2 ≥ 92%
PaO2 ≥ 8kPa
life threatening asthma
any of these ;
Grunting
Impaired consciousness, confusion, exhaustion
Bradycardia/ arrhythmia/ hypotension
PEF < 33% predicted or best
Cyanosis
Silent chest
Poor respiratory effort
SaO2 < 92% (definitely needs blood gas!)
PaO2 < 8kPa
PaCO2 normal (4.6 - 6.0kPa)
near fatal asthma
Raised PaCO2
Need for mechanical ventilation ( intubation and life support machine )
complete control of asthma
no daytime symptoms
no night time wakening
no need for rescue medication
no asthma attacks
no limitations on activity including exercise & normal lung function (in practical terms FEV1 and/or PEF>80% predicted or best)
minimal side effects from medication.
non pharmacological management of asthma in adults
Patient Education and Self management plans
Exercise
Smoking cessation
Weight management
Flu/Pneumococcal vaccinations
types of inhalers
metered dose inhalers which is used with spacers
dry powder inhaler
reliever medication in adults
short acting beta agonists example salbutamol
which is present in the dry powder inhaler and the metered dose inhaler
and terbutaline which is present in the dry powder inhaler only
pharmacological management
inhaled therapy
oral therapy
specialist treatments
oral therapy
Leukotriene Receptor Antagonist( montelukast )
Theophylline- very adverse
Prednisolone- acute
specialist options
Omalizumab (Anti- IgE)
Mepolizumab (Anti-Interleukin-5)
Bronchial thermoplasty
mild asthma attack in adults
Increase inhaler use
Oral Steroid
Treat trigger
Early follow up and Back up plan to check if the medication given is working
severe asthma in adults
Nebulisers – Salbutamol/Ipratropium
Oral/IV Steroid
Magnesium
Aminophylline
Triggers – infection/allergen
Complications – CXR
Review
Level 2/3 care
