pharmacology Flashcards
what controls the airways para or sympathetic
parasympathetic
is parasympathetic preganglionic Cholinergic or nitrergic
cholinergic
where do parasympathetic preganglionic fibres come from
brainstem
where do parasympathetic post ganglionic fibres act on
bronchioles
what are the neurotransmitters and receptors of the cholinergic fibres and what do they do
ACh and M3, M3 increases phospho C which converts IP2 to PIP3 which opens calcium channels
what are the neurotransmitters of the non-cholinergic fibres and what do they do
NO and VIP, dilation
what do sympathetic post ganglionic fibres act on
submucosal glands and smooth muscles of arterial vessels (a1)
what do sympathetic post ganglionic fibres act on, causing what to be released
adrenal glands, adrenaline
what receptors does adrenaline act on and what does this cause
B2, dilation, decreased mucous secretion, increased mucociliary clearance
which 2 ways can cause contraction in airway smooth muscle
hormonal (ACh on m3, causing IP3) and depolarisation (calcium influx), both cause Ca influx
how does calcium cause contraction
Ca binds to calmodium which activates myosin light chain kinase (MLCK), MLCK used ATP to phosphorylate MLC and myosin slides past actin
what caused relaxation of MLC
dephosphorylation of MLC by myosin phosphate (MP),
is asthma obstructive or restrictive and reversible or irreversible
obstructive, reversible
what are pathological changes of asthma
1) increased smooth muscle mass, 2) accumulation of interstitial fluid 3) increased mucous secretion 4) epithelial damage 5) sub epithelial fibrosis
What happens to FEV1 and peak flow in asthamtics
decrease
what causes hypersensitivity of airways
epithelial damage exposing nerve endings
what is the difference between mild and severe asthma
mild = hypersensitivity and minor hyperactivity, severe = hypersensitivity and hyper activity
why does hypersensitivity to an allergen mean
when allergen eg pollen is inhaled, there is a very strong immune inflammatory response
in non-atopic individuals what happens when pollen is inhaled
dendritic cell phagotyoses and TH0 cells produce TH1 (normally IgG
in atopic individuals what happens when pollen is inhaled
strong TH2 response, release interleukins (IL4) and activate B cells producing IgE
in severe asthma what T cells are involved
TH2 and TH1
what does IgE bind to
FcE on mast cells and eisonophils
what do mast cells and eisonophils release
leukotrienes, histamina and chemokines
what are the 2 components of an asthma attack
initial phase (bronchospasm and early inflammation), followed by delayed stage (inflammation and bronchospasm)
what cells cause early stage
mast cells
what cells cause late stage
eosinophils
what are the main relievers in asthma - bronchodilators
SABA’s, LABA’s, CysLT1 antagonist
what are the main controllers in asthma - anti-inflammatory
glucocorticoids and cromoglicate
what is both a controller and reliever
methylxanthines
what action to beta2 adrenoreceptor agonists have on ASM
cause relaxation by stimulating adenyly cylcase to increase cAMP which activates PKA which inhibits MCLK and activates MP
what are the types of beta2 adrenoreceptor agonists
SABA’s eg salbutamol, LABA’s eg salmenterol and formoterol, ultra-LABA
what is CysLT1 used for and an example
acute bronchospasm, taken orally, not for severe asthma. eg Montelukast, orally
what is known about methylxanthines
very narrow therapeutic window and lots of side affects eg Theophylline, orally
what are the 2 main classes or corticosteroids
glucocorticoids and mineralocorticoids, inhaled
what does cortisol do
decreased inflammatory and immunological response
what do mineralocorticoids do
salt and water retention
what is the action mechanism of glucocorticoids
bind to GRa and alter transcription of anti-inflammatory proteins, not bronchodilators
for chronic and severe asthma what is the last step before hospitalisation
prednisolone, orally, is a glucocorticoids
what are cromones used for
mast cell stabilisation, reduces inflammatory response, eg sodium cromoglicate
is COPD obstructive or restrictive and irreversible or reversible
obstructive, irreversible (sometimes reversible eg exacerbations)
COPD often branches into what 2 conditions
emphysema and chronic bronchitis
what is emphysema
Collapsing alveoli and loss of elastic recoil, losing SA for gas exchange, can cause SOB
what is chronic bronchitis
inflammation of bronchioles and bronchi, increased sputum production, can cause coughing and SOB
what does M1 do
allow transmission of ACh from pre to post ganglionic fibres (this allows contriction)
what does M3 do
allows ACh to activate constriction of ASM
What does M2 do
inhibits further release of ACh, (aids broncodilation)
what does SAMA act on and give an example
non selective of M1, M2 and M3, is inhaled, ipratropium
what does LAMA act on and give an example
inhaled, acts on M3, eg tiotropium
give an example of an ultra-LABA
Indacaterol
what does a PDE4 inhibitor do
supresses inflammation by acting on eosinophils eg Rofumilast
what is rhinitis
inflammation of nasal mucosa causing sneezing, rhinorrhoea (runny nose) and a blocked nose (common cold, hay fever)
what antibody is produced in allergic rhinitis
IgE
what drugs can be given for rhinitis
H1 and CysLT1 receptor antagonists, sodium chromoglicate and Glucocorticoids
what are H1 receptor antagonists more commonly known as
anti-histamines
