asthma medicine Flashcards
(17 cards)
asthma:
A — , — disease of the — characterised by — , — airway — .
This obstruction is due to a combination of three factors:
1- mucosal —- with inflammatory cells, ( — , — cells and — lymphocytes).
2- Neural — .
3-Smooth muscle — and — of the — membrane, the space below the — .
chornic inflammatory
airway
reverisble intermittent
obstruction
inflamamtion
estiophils , mast cells , th2
hyper-responsivness
hypertrophy and thickening
basement
epithelium
whys asthma important:
-300 million people worldwide.
-Affects 10-15% of — & 10% of — (U.K.)*.
-Accounts for large number of hospital presentations.
-Higher incidence in Western and Urban societies – This is likely a combination of greater exposure to — and greater access to — .
-Asthma caused 455,000 deaths [3 deaths per day in UK] in 2019 alone[1].
-Most asthma-related deaths occur in —and —- income countries, where under-diagnosis and under-treatment is a challenge[2].
children
adults
ateiologies and diganosis
lower and lower middle
pathophysiology:
-All symptoms are related to airway — secondary to airway —& smooth muscle —, which is a — process [—-,—- cells and— ].
-This immune dysregulation is driven by — ,—- and — .
-smooth muscle surrounding airway becomes — and — airway this reduces amount of air that can pass through leading to — .
-Airway epithelium becomes — , — and — .
Inflammatory mediators include:
Type2 T-helper lymphocytes, IL-4, IL-5, IL-13.
Eosinophils, IgE,Mast cells,Histamine,Leukotrienes.
obstruction
inflammation
contraction
mutlicellular
estiphils, mast cells , lymphocyte
pollution,allergen,viruses
oedematous
tightens
wheeze
oedematous , erythematous and inflamed
microscopic features:
-Airway infiltration by — and —.
- — degranulation.
- Basement membrane —.
- Loss of epithelial —.
- — of bronchial lumen by —.
- — and —- of bronchial smooth muscle and goblet cells.
estinophils and neurphils
mast cells
thickneing
integrity
occlusion
mucus
hyperplasia and hypertrophy
more info on pathogensis and aetology;
- all symptoms are related to airway — 2ndary to airway — smooth muscle contraction which is a mutlicellular process
- there are two inflammatory phenotype estiophilic asthma and nerophilic asthma
1- estinophilic asthma is associated w — of the basement memebrane and w steriod — , its a classic — asthma that involves interactions between IgE , th2 , mast cells and estinophils
2- neutrophilic asthma and its sub groups are steriod — and maybe associated w more — disease and poorly understood
- increased airway inflamation in response to insults reuslts in bronchial —- and — mediated by airway smooth muscle contraction
- this in return results in goblet cells — and increased — secretions
obstruction
inflammation
thickening
steriod responesvinsess
allergic asthma
steriod resistant
severe
hyper-responsivness
brochoconstricito
hypertrophy
mucus secretion
externsic asthma ( allergic , estinophilic)
Predominates in — .
individual or family history of — ( — , — , — ).
Increased — levels and — on skin testing
1- Antigen-induced asthma
* — type (30-50%)
* —- allergens - pollens, animal hair, house dust mite
2- Occupation-related
*— different substances identified, e.g. animal handlers, wood workers.
3- — pollution
*Sulphur dioxide, ozone
4- —-induced
*Aspirin, NSAIDs, Antibiotics &Beta-blockers
5- — respiratory tract infections
*Children - respiratory syncytial virus [RSV], influenza, rhinovirus
6- —-induced asthma
*Cold or humid air increases risk.
childhood
atopy ( allergy , eczema ,heyfever)
IgE
immediate hypersensitivity
commonest
airborn
80
environmental
drug
viral
excericse
intrisnic ( non allergic , non estinophilic) :
- —
- No individual or family history of — disease
-Skin/inhalation tests –
- Nasal —
- Drug hypersensitivity to — & —
-Often associated with —
-Prognosis – good
adults
atopic
-ve
nasal polyps
aspirin and penicillin
COPD
less
asthma symtoms:
Cough (often — )
Wheeze ( — )
Shortness of breath (—-)
Typically, first onset in — but can present as an –
Strong relationship with — and — ( —/ — )
nocturnal
intermittet
reverisble
childhood
asult
rhinitis and eczema
allergy , atopy
asthma history is important:
1- SOB
—- of symptoms (rapidity of onset)
Quantify — of shortness of breath (SOB)
—,—-
—- variation
Precipitating factors (on this occasion)
Associated—/ chest—/ —
Frequency of — usage
Also
Chest tightness/ Cough/ Wheeze
2- asthma past medical history :
When was asthma diagnosed?
-By whom? And How?
-Impact of asthma
-Progression over time
-Days off work or school/ annum
-Precipitating factors
3- asthma medication history:
-Current inhalers / Oral medications
-Adherence
-Frequency of-agonist usage (when well)
-Previous inhalers (explore reason for change)
duration
degree
episidoic , noctural
diurnal
wheeze , tightness , cough
b agonist
asthma : how much impact has the condition had in the past:
-GP / ED — per year
-Number of nebuliser — per year
-Number of courses of —per year
-Number of courses of — per year
-Previous hospital —.
-Previous Intensive Care Unit (ICU) admissions / Intubation (put on a ventilator machine to help breathing).
visists
prescirption
oral steriofs
antibitoic
admissions
levels of asthma control:
Characteristic
Controlled
(All of the following)
Partly Controlled
(Any measure present in any week)
Uncontrolled
Daytime symptoms
None (twice or less/week)
More than twice/week
Three or more features
of partly controlled
asthma present
Limitations of activities
None
Any
Nocturnal symptoms/awakening
None
Any
Need for reliever/
rescue treatment
None (twice or less/week)
More than twice/week
Lung function (PEF or FEV1)‡
Normal
< 80% predicted or personal best (if known)
Exacerbations
None
One or more/year*
One in any week†
asthma : system reviews
Medication side effects
1-Inhaled corticosteroids : —
2- b-agonists - –, —
3- Oral steroids : — , — , –, — , — , peptic — disease (PUD), — , easy —
oral candidiasis
tremor , palpitation
obesity , striae , myopathy , glacuoma , osteroprosis , ulcers , dibetes , bruising
asthma summary of features:
Classic triad:
- —
- —-
- — (Non-productive)
Diurnal pattern to symptoms: worse at – / early –
Presence of — triggers
- mechanism of symotms in asthma :
ifnlammation —> altered – acitvity and — —> reverisble airway — –> —- —> cough , wheeze , breathlessness
wheeze
dysponea
cough
night , early morning
identifiable
neural + hyperreactivity
narrowing
remodelling
asthma dirunal variation:
Plasma cortisol levels drop at —
Plasma adrenaline levels drop at —
Nocturnal symptom — onwards
*Generally, symptoms worst in the — and at —
- natural history of asthma - not precisely defined:
In majority of patients, it is not — (contrast with chronic bronchitis,emphysema, cystic fibrosis, bronchiectasis)
Some (minority) patients do develop — changes in – function
Clinical course is characterised by – and —
12 am
4 am
2-3 am
morning and night
not progressive
ireeveirsble
lung
remissions and exacerbation
differential diagnosis:
1- Other causes of airway obstruction / wheeze:
*COPD
*Bronchiectasis
*Cystic fibrosis
*Airway tumour
*Goitre(enlarged thyroid)
*Foreign body
*Anaphylaxis
2- Other causes of cough:
*Sinusitis and post-nasal drip
*Gastro-oesophageal reflux
*Bronchiectasis
*LRTI / Pneumonia
3-Other causes of dyspnoea:
*Pulmonary embolus
*Pneumothorax
*Heart failure
*Acute coronary syndrome
risk factors for exacerbation ( triggers) :
smoking
viral illness
air pollution
dust and dust mites
pets
hay fever
food allergeis
excericse
weather changes
key points:
Asthma is a common condition with variable — airflow — due to — of the airways
Episodic shortness of breath, cough and wheeze are the main symptoms
2 main types– Allergic ( — ) and Non-allergic (—)
Diagnosis and Treatment will be covered at a — stage. Treatment is focused on limiting — and relief of airway – .
intemittenet
limitation
inflamamtion
eostinophilic
non estinophilic
later
inflammation
obstruction
