week 9 Flashcards
how long does a persons asthma need to be well controlled for before it would be appropriate to reduce ICS dose?
6 months
which class of asthma would a patient who’s PEFR is 50-75% of their best- what would we do with their treatment?
moderate asthma
- increase regular therapy, or step up therapy if required
how is severe asthma classified? (4)
one of
- PEFR 33-50% of their best
- unable to talk in sentences due to breathlessness
- respiratory rate 25 or more
- pulse of 110 or more
how would we treat severe asthma (5)
- refer to hospital- may not always need admission
- oxygen 40-60% via venturi mask
- oral corticosteroid (prednisolone 40mg/day)
- nebulised SABA - salbutamol
- nebulised SAMA if required- ipatropium
how is life threatening asthma classified?
severe asthma and one of the following
- altered consciousness
- exhaustion
- arrhythmia
- hypotension
- cyanosis (blue lips etc)
- silent chest (shows no movement of air in the chest)
- poor respiratory effort
PEFR- less than 33% of best
oxygen less than 92%
how would we manage life threatening asthma?
- hospital admission
- nebulised beta antagonist and ipatropium- driving by oxygen
- oral corticosteroid (prednisolone)
- oxygen therapy
- IV aminophylline, salbutamol or terbutaline
- IV fluids and electrolytes- especially potassium
treatment for mild COPD exacerbation?
short acting bronchodilator (salbutamol)
treatment for moderate COPD exacerbation? (3)
salbutamol and antibiotics (normally amoxicillin, but can use doxycycline or clarithromycin if required) and/ or oral corticosteroid
treatment for severe COPD exacerbation?
admission to hospital may be required
- possible acute Respiratory failure so need monitoring for this
name 5 signs of a COPD exacerbation
- increased breathlessness
- increased cough
- increased sputum volume or purulence- also might be a yellow/ green colour if infection
- increased wheeze
-increased tightness in chest
why should nebulisers be driven by air and not oxygen in COPD exacerbations?
the patients body may be used to a low level of oxygen- if it suddenly increases very high the patient will stop breathing as their body thinks they have enough- COPD patients tend to breath to get oxygen rather than ‘normal’ people who breath to get rid of CO2
associate with type 2 respiratory failure
why is raising cAMP good?
inhibits inflammation- turns on anti inflammatory pathway, turns off pro inflammatory pathways
name 4 cell mediated effects of PDE4 inhibition
- smooth muscle relaxation
- TNF alpha release
- T cell proliferation
- chemotaxis
name 5 positive characteristics of roflumilast
- good bioavailability (~80%)
- reduced accumulation of neutrophils
- improved lung function in COPD patients
- few side effects
- weight loss associated
what is roflumilast?
a PDE4 inhibitor
how many chiral centres are in a steroid backbone structure?
6
which corticosteroids maintain salt balance and water retention?
mineralcorticosteroids
what do all biologically active adrenocorticoids require?
a 3-keto group and 4,5 unsaturation
name 4 reasons why tobacco is addictive
- nicotine changes brain chemistry
- dopamine reward pathway
- behaviour- situations linked with tobacco use
- emotional- becomes coping mechanism
social cognitive theory??
focuses on the role of observing and learning from others and on positive and negative reinforcement of behaviours
name 3 nicotine withdrawal symptoms- why is it important to be aware of these?
- irritability
- sleepiness
- anxiety
- anger
- sadness
- restlessness
- insomnia
so we can make patients aware and help them cope with these symptoms- we can offer help and support of dealing with them
what are the 5 Ds of coping with nicotine withdrawal ?
delay
distract
drink water
deep breaths
discuss
what makes a person suitable for NRT?
need to be nicotine dependent meaning
- having their first cigarette within 30 mins or waking
or
- smoke 10 or more cigarettes per day
or
- have craving and/or withdrawal symptoms in previous quit attempts
how does theophylline work?
- inhibits phosphodiesterase 3- which relaxes smooth muscle in the airways
- inhibits phosphodiesterase 4- which reduces mediator release form alveolar macrophages
- increases apoptosis of inflammatory neutrophils ad T cells
