CLASS ACTION METABOLISM INDICATIONS CONTRAINDICATIONS SIDE EFFECTS & TOXICITY

Long acting β2 agonist Stimulate adenylyl Act for 12-24hrs Long term control of Not sole treatment; -Skeletal muscle tremor
cyclase via β2 moderate to severe exacerbates mortality -Tachycardia
“-terol” adrenoreceptor Metabolism in gut asthma use in combination -Arrhythmia - ^K+ in cells, vK+
Albuterol pathway; increases wall with corticosteroids in blood
Terbutaline cAMP in smooth muscle MUST be combined Hypokalaemia
Metaproterenol cells to dilate with inhaled -Vasodilation – BP reduced with
bronchioles and lungs corticosteroids tachycardia
COPD -Pulmonary hypoxia –
Indactaerol Enhance anti- -Nocturnal asthma ventilation/perfusion mismatch
Olodaterol inflammatory effects of -AM/PM PEF variation
Vilanterol GCS -exercise induced Toxicity:
asthma -Atropine if bradycardic
-Glucagon if resistant
Short acting β2 agonist Stimulate adenylyl Act for <4hrs First line in acute Do not use for -Skeletal muscle tremor
cyclase via β2 asthma attacks prophylaxis; t ½ too -Tachycardia
“-terol” adrenoreceptor 2, 4, 8mg tablets short -Arrhythmia
Salmeterol pathway; increases Syringe – 2/5mg Intermittent asthma –
Formoterol cAMP in smooth muscle Inhaler – 100ug only medication for
cells to dilate Rotacaps – 200ug quick relief
Idacaterol - COPD bronchioles
Methylxanthines Degrades T ½ – 6-12 hrs Slow release Can cause arrhythmias -GIT irritation and motility;
phosphodiesterase; theophylline in CV patients increase in acid pepsin
Theophylline which breaks down Eliminated by P450 nocturnal asthma
Aminophylline cAMP in the liver Do not give above CNS stimulation
Pentoxiphylline -Causes increased cAMP Aminophylline 4mg/100ml  leads 1)improves performance and
(intermittent -Blocks adenosine Clearance ^ to CV problems and clarity
claudication) receptors  no smooth -Young age Pentoxifylline arrhythmias, 2)nervousness, insomnia,
muscle contraction -Smokers intermittent convulsions and coma restlessness
no histamine release -Liver inducers claudication 3)tremor, convulsions
reduces blood Taken with enzyme
Requires high Zero order (low viscocity inducers Cardiac stimulation;
concentrations for dose) phenobarbitone + Arrhythmias
effect First order (high) COPD: rifampicin Vasodilation and
Hydroxyethyl -Increases hypotension
Theophylline theophylline/ theophylline  cerebral vessel constriction –
oral Derriphylline with metabolism migraines
100/200mg Roflumilast (PDE4 -Reduces t ½ of
inhibitor) for COPD theophylline CV TOXICITY REVERSED WITH
Aminophylline BETA BLOCKERS
oral/IV -Bronchial asthma Enzyme inhibitors – Adenosine causes
100mg tablets -COPD erythromycin bronchoconstriction from
250mg IV -Infantile apnoea -Decreases bronchial tone
theophylline
Hydroxyethyl metabolism Kidney
theophylline -Inreases t ½ of diuresis; v Na+ absorption;
oral/IV theophylline ^GFR/RBF
100/300mg
tablets Plasma fatty acid level
220mg/2ml IV increases
Muscarinic antagonists Block muscarinic Minimally absorbed Acute asthma – quick Glaucoma – ciliary Acetylcholine causes increase in
Anti-cholinergics receptors (M3) in the Direct application to relief muscles in the eye can activation of muscarinic
airways and mucosal airway relax and obstruct receptors
“-tropium” glands; Refractory asthma  flow in patients with
Ipratropium prevents attachment of Ipratropium – Salbutamol + glaucoma
Tiotropium ACh; stops contraction poorly absorbed Ipratropium
Aclidinium across mucosal Peptic ulcers
Prevent bronchodilation membranes COPD  GI tract obstruction
Prototype: from cholinergic inhaled: 30mins Albuterol +
Atropine parasympathetic lasts 6 hrs Ipratropium Chronic inflammation;
autonomic stimulation binds to M3 and has no effect
from vagus ganglia in M2 Salmeterol +
large/medium airways MDI or nebulizer Tiotropium

M1- peribronchial Aclidinium – Less effective than B2

ganglion Dissociate from M2 blockers in asthma
M2 – postganglionic quickly; selective for
nerves, activated by M3 More effective/less
ACh; promote reuptake toxic in COPD
into nerve terminal bronchospasm
M3 – smooth muscle
M3  ^ cAMP –
blocked M3 causes
cAMP reduction

Do NOT affect chronic

inflammation
Cromolyn and Decreases release of Aerosol - asthma Asthma – prevents Acute asthma attacks -Cough
Nedocromil inflammatory mediators allergic – has no direct effect -Irritation of airway
eg. Leukotrienes, Nasal – hay fever bronchoconstriction on bronchodilation -Drug allergy
histamine
Oral – food allergy Hay fever – prevents
inflammation of
nasopharynx
 Prevents allergic/ IgE
mediated reactions in Food allergy
bronchoconstriction,
Conjunctiva,
nasopharynx
Corticosteroids Inhibit phospholipase Onset at 2-4 weeks Moderate to severe: Effects are NOT -Adrenal suppression
A2 Reduce synthesis of use inhaled curative, but are -Growth retardation
“-sonide” of arachnidonic acid  first line preventative -Osteoporosis
Beclomethasone inhibits COX-2 Beclometh – 250ug -Glucose intolerance
Budesonide expression  Status asthmaticus -Behavioral changes: insomnia,
Ciclesonide prostaglandin and Budesonide – 200ug (fatal) mania, depression, psychosis
Flunisonide thromboxane inhibited intravenous -Glaucoma
 reduces Fluticasone prednisolone & -Infection subsceptibility 
IV drugs: inflammation proprionate – 100ug hydrocortisone candidiasis infection
Prednisolone
Hydrocortisone Ciclenoside – 80ug Progressive chronic
Methylprednisolone hydrolysed by asthma
bronchial esterases if unresponsive to
to Des-Ciclesonide previous treatment
Mineralocorticoids 120x affinity
“-cortisone”
Glucocorticoids Bind to intracellular Moderate-severe: Moderate to severe: Do not continue -Cushing’s syndrome
receptors  activate inhaled inhaled >40mg per day for -Osteoporosis
“-methasone” glucocorticoid response first line longer than a week -Immunosuppression
elements (GRE) in the Status asthmaticus: -Impaired glucose regulation
nucleus  prevents IV Status asthmaticus Does NOT -Peptic ulceration
synthesis of (fatal) bronchodilate; is an -Hyperlipidaemia
inflammatory cytokines Maximum action intravenous anti-inflammatory -Fluid retention
when taken long prednisolone & -Hypertension: vascular and
Leukotrienes from term 9-12 months hydrocortisone cranial
eicosanoid synthesis Parenteral steroids
reduced)
 Decreases -
Prostaglandins
-WBC infiltration
-capillary permability
-Ab/Ag reactions

Increases –
B2 receptors
Effect of B2 agonists

Leukotriene Block LTD4 and LTE4 Oral Paediatrics; offered at Do not use for: -Churg-Strauss syndrome –
antagonists receptors -orally absorbed lower dose Severe acute asthma eosinophilic granulomatosis
blocks cytokine attacks – has no effect with polyangiitis; necrotizing
“-lukast” production and Plasma protein Exercise induced fasciculitis of vessels with
Montelukast  blocks phagocyte / bound asthma severe asthma and pulmonary
Zafirlukast eosinophil attraction infiltrates
 prevents T1/2 Mild/moderate
bronchoconstriction Montelukast -3-6hrs asthma
and inflammation Zafirlukast – 8-12hrs
Allergen
Cysteinyl leukotrienes: induced/allergic
LTB4 reaction
LTD4
LTE4 NSAID/Aspirin
induced –
Prevents leukotrienes when inhibition of
from acting on tissues COX-1 causes
decrease in
prostaglandins and
thromboxane, and
overcompensation of
leukotrienes occurs
Lipooxygenase Inhibits 5-lipoxygenase Elevation of liver enzymes
inhibitor  prevents conversion
of arachnidonic acid to
“-teuton” leukotrienes 
Zileuton prevents exercise and
allergen induced
bronchospasm

Prevents formation of
leukotrienes
Anti IgE monoclonal Binds to IgE on Therapy for 10 Adults/children older -Bronchospasm
antibody; sensitized mast cells  weeks than 12 years -Rash
prevents effect  -Arthralgia
“-mab” prevents release of Moderate-severe -Thrombocytopenia
inflammatory granules asthma
Omalizumab

Mast cell stabilizers Stabilize mast cells Synthetic Prophylaxis of asthma Acute asthma; has no
inhibit degranulation effect
Sodium cromoglicate of mast cells and MDI – 1mg/dose Allergic rhinitis
Ketotifen inflammatory responses 2 puffs 4xdaily
Allergic conjunctivitis
Reduces inflammatory
mediator release
Prevents chemotaxis
of eosinophils/
neutrophils

Delays Cl- channel in

mast cell membrane

Long term – prevents

bronchial hyperactivity
Epinephrine Onset – 15 mins Anaphylaxis or allergic Hypertension -Hyperglycaemia
asthma - severe Heart failure -Tachycardia
Duration – 60-90 comorbidities -Arrhythmias
mins/ 1-2 hrs
Poorly controlled
Inhaled or SC diabetes – worsened
- Not oral by hyperglycaemia
PEFR 100%  Inhaled short acting β2 agonist  Salmeterol, Formeterol

PEFR <80%  SABA + inhaled low dose corticosteroid  Salmeterol + Ciclosenide/Beclomethasone

PEFR 50-80%  SABA + inhaled corticosteroid + inhaled LABA

uncontrolled; add Leukotriene receptor agonist/Theophylline  Sal + Cicle + Albuterol

increase inhaled corticosteroids 200ug daily

PEFR <50%  Add prednisolone  Sal + Cicle + Albuterol + 40mg prednisolone

PEFR <30%  Hospitalised  Nebulized salbutamol + IV corticosteroids 

ACUTE ANAPHYLAXIS  Epinephrine + LTAG + Cromolyn

COPD  Muscarinic receptors

Extrinsic/allergic  Atopy + allergies

POSITIVE skin test

^ IgE

<30 years old

 LESS prone to Status Asthmaticus

Intrinsic/ idiosyncratic No allergy

NEGATIVE skin test

IgE stays the same

>30 years old; middle aged

PRONE to SA
COPD defined by low FEV1 value

-Does not acutely respond to bronchodilators while asthma does

AIRWAY TONE:

-Controlled by parasympathetic fibres of vagus nerve

-Tonically active, produce reversible baseline airway tone

-Smooth muscle contraction mediated by M3; induced by ACh

-M3 mAChRs – mucous secretions and vasodilation

Bronchodilators:

- B2 agonists – salbutamol, bitolerol, torbutaline, salmeterol

-Epinephrine

-Adrenaline

-Methylxanthines – theophylline, aminophylline

-Anticholinergics – ipratropium bromide and tiotropium bromide