RESP ashtma Flashcards
what are three characteristics of asthma?
- airflow limitation
- airway hyper-responsiveness
- Bronchial inflammation
what causes inflammation in airways?
- Increase in mast cell mediated release of histamine, tryptase, PGD2 and cytokines
- increase eosinophils in the bronchial wall releasing LTC4
- Increase CD4
what are the results of lung function tests in asthma?
- peak expiratory flow rate before and after using a bronchodilator
- spirometry will show an obstructive condition
what is the step wise management of asthma?
- SABA
- Low dose corticosteroids
- +LABA
- +high dose inhaled corticosteroids and regular bronchodilator
- oral corticosteroid
how are SABAS used in asthma?
Salbutamol 100mg. Can be used in any step
when are inhaled low dose corticosteroids used in asthma treatment?
From step 2 (with SABA)
what are unwanted effects of inhaled corticosteroids?
oral candidiasis
hoarseness
What are signs of an asthma attack?
- inability to complete a sentence in one breath
- RR>25
- tachycardia >110
- PEFR<50%
what is management of an asthma attack?
Nebulised SABA
CXR to exclude causes
oral prednisolone
how does SABA work?
A beta 2 agonist
smooth muscle relaxation on the bronchi
what are the major side effects of SABA?
tachycardia fight or flight effects - palpitations - anxiety -tremor
how do leukotriene antagonists work?
- bronchodilator and anti inflammatory effect
- stop the formation of LTC4,LTD4,LTR4 which are all pro inflammatory
what drug should you not give an asthmatics?
NSAIDS especially COX 1 specific
Beta blockers (bronchoconstriction)
what is the emergency management for life threatening asthma?
Nebulised oxygen and salbutamol Hydrocortisone
Ipratropium
Magnesium sulphate if they get resp acidosis
what is the role of NIV in the management of acute asthma?
It has no place here
what are features of severe asthma?
- peak flow 33-50% of predicted
- RR>25
HR >110 - Can’t complete sentences
what are features of life threatening asthma?
- peak flow <33% predicted
- oxygen sats <92%
- hypoxic
- silent chest cyanosis
- bradycardia
- hypotension
- exhaustion
- confusion
what is the emergency management of asthma for someone coming into A and E?
O- nebulised oxygen S-salbutamol H- hydrocortisone I- ipratropium M- magnesium sulphate if they get resp acidosis T-theophiline
what symptoms are experienced by people with COPD?
- COB
- productive cough
- increased sputum
- frequent bronchitis
- pursed lipped breathing
- red faced
what are the systemic symptoms of COPD?
- cachexia
- increased CRP leading to increased CVS risk
- normochromic normocytic anaemia
- systemic inflammation
what clinical signs are found in people with COPD?
- nicotine stained fingers due to heavy smoking
- pursed lip breathing
- breathing with accessory muscles
- barrel chested
- reduced expansion
- crackles
- soft heart sounds
- hypercapnia
- hyperinflation
- liver problems if there is an AAT deficiency.
what anatomical changes are involved in the pathophys of COPD?
Proximal airways:
- trachea and cartilagenous airways become enlarged >2mm due to submucosal bronchial enlargment, squamous metaplasia of the airway epithelium and increased smooth muscle
The peripheral airways become <2mm as there is increased macrophages ND FIBROBLASTS.
- alveolour wall destruction and emphysema
where is centrilobular emphysema?
Main in the upper lobes associated with smokers.
what is panacinar emphysema?
Destruction of the acinus seen in AAT deficiency. affects the lower zomes
what are the three main processes in COPD development?
- inflammation
- protease and anti-protease imbalance
- oxidant and anti oxidant imbalance
what is the inflammation seen in COPD?
- cigarrete smoke activates macrophages and epithelial cells
- release of chemotactic factors
- recruitment of neutrophils and CD8 (CD8>CD4)
- activation of fibroblasts
- abnormal repair and bronchiolar fibrosis
What is the problem of the increased protease activity in COPD?
they lead to increased alveolour wall destruction and cause mucous release
what proteases are released from neutrophils in COPD?
elastase, cathepsin G, protease 3
what proteases come from macrophages in COPD?
cysteine protease
cathepsins EALS
what are the main ant proteases that you lack in COPD?
AAT#secretory leucoprotease inhibitor
tissue inhibitor of MMP
what causes the increased oxidative stress in COPD?
activation of antiproteases, stimulation of mucous production
oxidants come from cigRETTE SMOKE.
what are some causes of COPD?
AAT1 deficiency smoking ashtma/ airway hyperactivity recurrent infections dust mining
what spirometry figures are for mild airflow obstruction in COPD?
FEV 50-80%
what spirometry figures are for moderate airway obstruction in COPD?
FEV: 30-49%
what spirometry figures are for severe airway obstruction in COPD?
FEV <30%
what may be seen in a chest xray of a COPD patient?
hyperinflation of the lungs
flattening of the diaphragm
bullae
large proximal vessels
what can be seen in the ECG of a COPD patient?
RVH
right axis deviation
big P waves
what main drugs are used in smoking cessation?
bupropion/zyban
varenicline/ chantix
Cytisine
what is bupropion?
Used for smoking cessatation and reduces cravings
what are side effects of bupropion?
dry mouth
problems sleeping
behaviour changes
who shouldn’t take bupropion?
pregnant
under 18
what is varenicline?
Oral partial agonist of nicotonic Ach receptor to reduce withdrawal and craving.
what are types of bronchodilators?
Beta agonists
Anti cholinergics
what are examples of SABA used in COPD?
anti cholinergic: ipratropium
Beta 2: albuterol
why are corticosteroids used in COPD?
to improves symptoms, lung function and aid chronic inflammation
what is the problem of giving corticosteroids in COPD?
increased risk of pneumonia
what is theophyline?
A bronchodilator that blocks conversion of Camp.
what are adverse effects of theophylline?
nausea hypokalaemia abdominal pain headache diarrhoea
what are complications of COPD?
Cor pulmonale Depress Resp failure Increased infections Polycythaemia Pulmonary hypertension
what causes cor pulmonale in COPD?
Pulmonary hypertension due to peripheral vascular constriction. this leads to right ventricular hypertrophy.
what is the main organism respinsible for infection in COPD?
haemophillus influenzae B
why can COPD patients get polycythaemia?
COPD causes hypoxia causes excess EPO leading to increased red blood cells
what is the emergancy maanagement in a patient presenting with IECOPD?
- sit up
- stop any sedatives
- salbutamol (bronchodilator)
- ipratropium
- antibiotics
- corticosteroids
what is the oxygen target in COPD?
88-92%
what organisms are common in COPD patients?
haemophilus influenzae B
Strep pneumonia
moraxella catarhallis
what are the consequences of hypoxia?
Polycythaemia cerebral ischaemia myocardial ischaemia tumour angiogenesis pulmonary vasoconstriction Peripheral vessel vasodilation