respiratory Flashcards
Beta 2 agonists:
- short acting examples? 2
- long acting examples? 2
- mechanism of action? (incl type of receptor)
- salbutamol
- terbutaline
- salmeterol
- formoterol
Beta 2 receptors are GPCR
agonists (like adrenaline) act on these receptors on smooth muscle cells -> smooth muscle relaxation in bronchioles -> open airways
“fight or flight, need open airways to get air in when running”
nb also stimulate Na+/K+ ATPase pumps -> shift of K+ into cells
- so can be used to treat hyperkalaemia (esp when IV access difficult) - but effect is not reliable so should be used alongside other stuff
Beta 2 agonists:
- short-acting examples? 2
- long-acting examples? 2
- indications (be specific re types used) 3
- terbutaline
- salbutamol
- formoterol
- sameterol
1) asthma (short-acting used in step one, long-acting also used in step 3, but only after step 2 - inhaled steroid)
2) COPD (1st line: short acting, 2nd line: long-acting)
3) hyperkalaemia (short acting used alongside, insulin, glucose + calcium gluconate) for urgent treatment
Beta 2 agonists:
- examples (2 short, 2 long)?
- contraindication? 1
- terbutaline
- salbutamol
- formoterol
- salmeterol
take care in patients with cardiovascular disease as may induce:
- angina
- arrhythmias
long-acting MUST be co-prescribed with corticosteroids, otherwise asthma deaths are increased
Beta 2 agonists:
- examples (2 short, 2 long)?
- common side effects? 4
- side effect specific to long-acting? 1
- terbutaline
- salbutamol
- formoterol
- salmeterol
- palpitations
- anxiety
- tremor
- tachycardia
nb also promote glycogenolysis -> increase blood glucose + at high doses: serum lactate may also rise
- “as it would if you were running a marathon = adrenaline/fight/flight”
- muscle cramps (w long-acting)
Beta 2 agonists:
- examples (2 short, 2 long)
- interactions? 2
- terbutaline
- salbutamol
- formoterol
- salmeterol
- Beta blockers may reduce effect of drug
concomitant use of: - high dose neb B2 agonist - theophylline - corticosteroids can -> hypokalaemia (so monitor K+ level)
Beta 2 agonists:
- what teach patient? 3
- how make sure steroid is also taken (for long acting)?
- what use in emergency?
- how to use inhaler
- that it just relieves breathlessness, but doesn’t treat underlying disease
- if using a lot/not well controlled, go back to dr and step up ladder
nb can give spacer to kids etc as easier to use than inhaler
- prescribe inhaler which contains BOTH steroid and long-acting
- use nebuliser in emergency
anticholinergics:
- examples? (1 short-acting, 2 long)
- suffix?
- mechanism of action? (incl what inhibit)
- abbreviation for long-acting?
- ipratropium
- tiotropium
- glycopyrronium
-(trop)ium
antimuscarinics are competitive inhibitors of acetylcholine (rest + digest)
- so dull down parasympathetic effect -> relative sympathetic effect (dilated bronchioles, faster heart rate etc)
“Beta 2 agonists increase sympathetic pathway, these reduce parasympathetic pathway”
long-acting anti-muscarinics
= LAMAs
anticholinergics:
- examples? (1 short, 2 long)
- indications? 2 (incl type used which line)
- ipratropium
- tiotropium
- glycopyrronium
1) COPD (long + short-acting used)
2) asthma (short used for acute exacerbations - w salbutamol - long used as 4th line, alongside steroids + long-acting B2 agonists)
anticholinergics:
- examples? (1 short, 2 long)
- relative contraindications?
- ipratropium
- tiotropium
- glycopyrronium
patients at risk of:
- acute angle-closure glaucoma (can raise intra-oc pressure)
- arrhythmias
nb in practise patients can inhale these drugs with no problems
anticholinergics:
- examples? (1 short, 2 long)
- side effect? 1
- interactions?
- ipratropium
- tiotropium
- glycolpyrronium
- dry mouth
“parasympathetic system produces secretions, so blocking this -> dry mouth”
nb for inhaled anticholinergics, get no other side effects (like constipation etc) as such low conc in blood stream
- interactions are not usually a problem due to low systemic absorption
anticholinergics:
- how to prevent side effect? 2
- what teach patient? 3
prevent dry mouth
- chew sugar free gum or suck sugar-free sweets
- drink plenty of water
- how to use inhaler
- that it just relieves breathlessness, but doesn’t treat underlying disease
- if using a lot/not well controlled, go back to dr and step up ladder
corticosteroids (inhaled):
- examples? 3
- suffix?
- mechanism of action (incl type of receptor)
- beclometASONE
- fluticASONE
- budesonide
- asone
- interact with nuclear receptors (lipophilic) to modify transcription of genes (anti-inflam are unregulated, pro-inflam are down-regulated)
- reduces mucosal inflammation
- widens airways
- reduces mucus secretions
corticosteroids (inhaled):
- examples? 3
- indications? (incl step)
- beclometASONE
- fluticASONE
- budesonide
1) asthma (step 2, after short-acting B2 agonist)
2) COPD (further down line, improve symptoms and prevent exacerbations)
corticosteroids (inhaled):
- examples? 3
- relative contraindications? 2
- interactions?
- beclomethASONE
- fluticASONE
- budesonide
- COPD w history of pneumonia (as surpasses immune reaction)
- Children (as can suppress growth)
- none clinically significant (for inhaled!!)
corticosteroids (inhaled):
- examples? 3
- adverse effects? 3
- systemic adverse effects (at high dose)? 3
- beclamethASONE
- fluticASONE
- budesonide
- oral thrush
- hoarse voice
- increase risk of pneumonia
- growth retardation (in kids)
- adrenal suppression
- osteoporosis
corticosteroids (inhaled):
- what teach patients?
- dose regularity?
- how to prevent side effects?
- how to use inhaler
- that it dampens down inflammation in lungs
- if using a lot/not well controlled, go back to dr and step up ladder
- norm twice a day
- rinse mouth + gargle after using (prevent thrush + sore throat)
corticosteroids (systemic):
- examples? 3
- suffix?
- mechanism of action? (incl receptor)
- prednisalONE
- hydrocortiSONE
- dexamethaSONE
-(s)one
interact with nuclear receptors (lipophilic) to modify transcription of genes (anti-inflam are unregulated, pro-inflam are down-regulated)
- direct action on inflammatory cells include suppression of circulating monocytes and eosinophils
metabolic effects include:
- increased gluconeogenesis -> breakdown of muscle + truncal obesity
nb mainly have glucocorticoid effects, but have some mineralocorticoid effects:
- stimulate Na + water retention + K excretion in kidneys
corticosteroids (systemic):
- examples?
- types of indication? 4
- dexamethaSONE
- prednisalONE
- hydrocortiSONE
1) allergic or inflammatory disorders (anaphylaxis, asthma)
2) autoimmune disease suppression (IBD, inflammatory arthritis)
3) some cancers (to reduce tumour-associated swelling)
4) hormone replacement (adrenal insufficiency or hypopituitarism)
corticosteroids (systemic)
- examples? 3
- relative contraindications? 2
- dexamethasone
- prednisalone
- hydrocortisone
- people with infections (suppress immune system)
- children (suppress growth)
corticosteroids (systemic) adverse effects: - immune? 1 - metabolic/catabolic? 7 - psychological? 4 - mineralocorticoid? 3 - hormonal/adrenal? 1
immune
- infection (increased risk)
metabolic/catabolic
- type 2 DM
- truncal obesity
- osteoporosis
- proximal muscle weakness
- skin thinning
- easy bruising
- gastritis
“catabolism means break down of tissue (all above are symptoms of this)”
psychological
- insomnia
- confusion
- psychosis
- suicidal ideas
mineralocorticoid:
- HTN
- hypokalaemia
- oedema
hormonal/adrenal:
- adrenal atrophy (secondary to ACTH suppression by exogenous steroid) - if taken off suddenly, can provoke an addisonian crisis with CVS collapse
“all of these side effects are side effects of stress - cortisol is ‘stress hormone’”
corticosteroids (systemic):
- examples? 3
- interactions? (+ effects) 4
- dexamethasone
- prednisalone
- hydrocortisone
NSAIDS
- increase risk of PUD + GI bleeding
B2-agonists, theophylline, loop or thiazide diuretics
- increase risk of hypokalaemia
cytochrome P450 inducers
- reduce efficacy of steroid
vaccines
- reduce immune response to vaccines
corticosteroids (systemic):
- examples? 3
- which most/least potent of the above?
- time of day taken?
- what to tell patients? 2
- long-term risks to tell patients? 2
- drugs which can be co-prescribed to reduce risk of long-term side effects? 2
- monitoring for long-term use? 2
- prednisalone (weakest)
- hydrocortisone
- dexaMETHasone (strongest)
“METH is a STRONG drug”
- morning (to mimic normal cortisol production + prevent insomnia)
- don’t stop suddenly (w prolonged treatment)
- may take a couple of days to see effect
- diabetes
- osteoporosis/bone fractures
nb make sure to talk through + weigh risk and benefits
- PPIs
- bisphosphonates
- DEXA scan
- glucose/HbA1c
nb give lowest dose for shortest time to decrease risk of side effects
mucolytics:
- example?
- mechanism of action?
- most common indication?
carbocysteine
- reduce viscosity of sputum
- COPD (also things like CF)
nb stop if no effect after 4 weeks
mucolytics:
- example?
- contraindication? 1
- side effects? 2
- interactions?
carbocysteine
- peptic ulcer disease (or high risk of)
- GI disturbance (diarrhoea etc)
- GI bleed
nb it damages the mucosal lining of gut
nb may also very rarely cause allergic reactions
no known interactions
