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Flashcards in Respiratory drugs and analgesics Deck (49)
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NSAIDs cellular pharmacodynamics

Irreversible, non-selectively inhibits COX enzymes preventing production of prostanoids. 


Systemic pharmacodynamics of NSAIDs


Due to decrease in PGE2 and prostacyclin causing reduced vasodilation and oedema. 


Due to decrease prostaglandin production and thus less sensitisation of nociceptive nerve endings to inflammatory mediators such as bradykinin. 

Antipyretic as NSAIDs prevent IL-1 activating COXs in the CNS which produce prostaglandins which raise the hypothalamic set point. 


Aspirin analgesic dose

300-900mg every 4 hours. 


Contraindications of NSAIDs

Beware 'tripply whammy' combination of ACEI/ARB + diuretic + NSAID causing acute renal failure. 


Children <12 years due to risk of Reye'ssyndrome when taen during a viral illness. 


Adverse drug reactions of NSAIDs

GI bleeding: due to inhibition of COX1 which normally provides prostaglandins to maintain themucosal lining of the stomach. 

Ibuprofen is 'gentlest' on the stomach. 

Cardiovascular events


Selective COX-2 Inhibitor indications

Long term pain relief (arthritis, dysmenorrhea)


NSAID and COX-2 inhibitor comparison

While COX-2 theoretically cause fewer GI side effects than non-selective NSAIDs, CLASS trial showed no real difference. 

Rofecoxib did show fewer GI side effects, but 5x more MI. 


Cellular pharmacodynamics of COX-2 Inhibitors

Selectively inhibits COX-2 enzymes avoiding adverse effects. COX-2 is thought to be responsible for the most inflammation, pain and fever; wile adverse effects are throught to be mosty due to inhibition of COX-1 (housekeepning enzymes).


Contraindications to COX-2

Any CVD hisory. 


Adverse drug reactions of COX-2 Inhibitors

Cardiovascular events: due to inhibitionof COX2 - this is predominantly responsible for producing PGI2 which normally inhibits platelet aggregation. 


Decongestants indications

Acute and chronic rhinitis


Decongestants cellular pharmacodynamics

Sympathomimetic amines. Agonise alpha adrenoreceptors on smooth muscle in the respiratory tract, producing vasoconstriction of dilated nasal vessels. 


Decongestants systemic pharmacodynamics

Reduces tissue hyperaemia, oedema and nasal congestion. 


Contraindications to decongestants

HTN, coronary artery disease (arrhythmias)


Adverse drug reactions of decongestants

Hypertension, tachycardia, palpitations, CNS stimulation, insomnia, tremor etc


Antitussives indications

Dru cough - opioid dervicatives 

Productive cough - expectorants, demulcents, muclytics. 

Investigate underlying disorder as coughing is usually desirable! Stop smoking. 


Cellular pharmacdynamics dry cough antitussives

Activate neuronal G-protein coupled oiioid receptors, inhibit adenylate cyclase, reducing cAMP levels and activating K+ channels hyperpolarising neuron. This reduces release of substance P, which is a neurokinin binding NK-1 which activates the cough centre in the medulla. 


Expectorant antitussive cellular pharmacodynamics

Thought to promote bronchial secretions, ciliary action and productive coughing by irritant action on mucosal membranes. 

May also soothe by lubricating dry tissues. 

Mainly placebo affect, 


Demulcents cellular pharmacodynamics

For productive cough. 

Thought to suppress coughs by forming a protective layer over sensory receptors in the pharynx. 


Mucolytics cellular pharmacodynamics

Acetylcysteine reduces mucus viscosity by splitting disulfide bonds in mucoproteins, bromhexine thought to improve mucous flow by enhancing hydrolysing activity of lysosomal enzymes. 


Systemic pharmacodynamics antitussives

Opioid derivates reduce frequency of dry, irritating cough.

Expectorants increase mucous production and movement

Demulcents suppress coughing

Mucolytics reduce mucus viscosity and aid its digestion


Antitussive contraindications

Opioids in respiratory failure, asthma and COPD and children <2 years. 


Adverse drug reactions antitussives

Opioids may cause opioid dependence, lethargy, stupor etc. 

Expectorants and mucolytics may cause nausea, vomiting and abdominal pain. 


Histamine antagonsists indications

Allergic rhinitis, chronic urticaria


Histamine antagonists cellular pharmacodynamics

Cellular: selectively antagonise the action of histamine at H1 receptors in both CNS and periphery. Histamine released from mast cells and basophils causes local inflammation, smooth muscle contraction and blood vessel dilation. Older 'drowsy' drugs penetrate blood brain barrier well and so cause CNS sedation, cognitive impairment and motor retardation. Newer, less sedating drugs do not penetrate the blood brain barrier well 


Systemic pharmacodynamics of histamine antagonists

Suppress symptoms of allergies such as runny nose and watery eyes. 


Histamine antagonists contraindications

Children <2 years


Adverse drug reactions to histamine antagonists

Drowsiness, fatigue (ever newer drugs to some extent)


Inhaled beta angonists indications

Acute asthma, COPD. 

'Relievers' and 'Symptom controllers'


Inhaled beta agonist comparison


SABAs are first line treatment in acute asthma. If needed >2 times a week, preventative treatment should be used. 

Step 2 is an ICS

Step 3 is ICS + LABA

Step 4 is other symptom controllers

In acute exacerbations, an oral corticosteroid may be used.