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Drugs affecting the respiratory system Flashcards

1
Q

Overview of the respiratory system

A
  • Nasal cavity warms, humidifies and cleans inspired air thereby protecting surface from dehydration, temp changes and pathogens
  • Diaphragm expands pleural cavity and sucks air from external environment towards gas exchange surfaces
  • Bronchial tree transmits air to bronchioles= main area of resistance to airflow
  • Alveoli= large s.a.
  • Vascular supply matches perfusion to ventilation and epithelium major site of ACE
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2
Q

What is asthma?

A
  • Paroxysmal, reversible airway obstruction (bronchoconstriction)
  • Caused by airway inflammation and bronchial hyperactivity
  • With variability in symptoms and lung function
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3
Q

What are the symptoms of asthma?

A
  • Breathlessness (chest tightness)
  • Wheeze
  • Cough
  • Diurnal variability (worse in the morning or at night)
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4
Q

What are the provoking factors of asthma?

A
  • Exercise/ hyperventilation
  • Food, additives
  • Drugs (NSAIDs, beta-blockers)
  • Cigarette smoke
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5
Q

Describe asthma rescue treatment

A

-Hypoxia (poor gas exchange):
=Oxygen
-Bronchoconstriction:
=Beta 2 agonists (salbutamol)= bronchodilator rapidly reduce airway obstruction, not 100% specific so risk activating beta 1 receptors in heart/ beta 2 receptors in muscle so inhaled medication reduces systemic effects
-Airways inflammation:
=Corticosteroids (prednisolone orally, hydrocortisone IV)= used to stabile severe attacks, few hors for apparent effects

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6
Q

What is COPD?

A
  • Inflammatory response of lung to prolonged exposure to noxious particles (cigarette smoke, cannabis, dust exposure)
  • Reversible and non-reversible airflow limitation (poor ventilation)
  • Damage to small airways and alveolar spaces (poor gas exchange)
  • Excess mucus production
  • Recurrent infection
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7
Q

What are the non-pulmonary complications of COPD?

A
  • Right heart failure (cor pulmonale)
  • Peripheral oedema
  • Weight loss
  • Muscle wasting
  • Osteoporosis
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8
Q

How do patients with COPD present?

A
  • Chronic bronchitis= cough producing sputum most days for 3 months over 2 consecutive years
  • Emphysema= enlarged air spaced distal to terminal bronchioles
  • Bronchiolitis= fibrosis and inflammation of small airways
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9
Q

What are COPD risk factors?

A
  • Smoking
  • Occupation
  • Recurrent infections
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10
Q

What are the signs of COPD?

A
  • Resting RR> 20 breaths/min
  • Accessory muscles
  • Pursed lipped breathing
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11
Q

How is COPD managed?

A 
-Lifestyle changes
=Smoking cessation
=Exercise based pulmonary rehabilitation
-Pharmacological
=Oxygen
=Bronchodilators (beta 2 agonists, antimuscarinic, theophylline)
=Corticosteroids (prednisolone)
-Antibiotics
-Surgical
=Bullectomy, transplant
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12
Q

What are the NICE COPD guidelines?

A 
-Mild (FEV1 50-80%)
=Inhaled anticholinergic/ beta 2 agonist
-Moderate
=Regular anticholinergic/ LABA (long acting beta agonist) plus inhaled corticosteroids
-Severe (FEV1<30%)
=Regular anticholinergic plus LABA plus inhaled steroid
=Oral corticosteroids (trial)
-PaO2 < 7.3 kPa
=Consider home O2
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13
Q

What are the drugs used to treat asthma and COPD?

A
  • Beta 2 agonists (salbutamol)
  • Anti-muscarinic drugs (ipratropium bromide)
  • Xanthines (theophylline)
  • Mast cell stabilising drugs (cromoglicate)
  • Leukotriene antagonists (Montelukast)
  • Corticosteroids (prednisolone)
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14
Q

Describe beta-adrenoceptors

A
  • Sympathetic NS (T4 to T7)
  • Beta 1= adrenoceptors. Heart= increased force and rate of contraction
  • Beta 2. Lung= relaxation of smooth muscle surrounding bronchi and bronchioles, increased diameter, reduces air flow resistance and improves ventilation of alveoli, increases effectiveness of O2 and CO2 exchange. Blood vessels= vasodilation
  • Beta-adrenoceptor antagonists used in heart disease may precipitate bronchospasm and are contra-indicated in asthma and COPD
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15
Q

What are the Beta 2 agonist effects?

A

-Smooth muscle in uterus, bladder, GI, airways (relaxation)
=Activation of beta 2 G-protein couple receptors
=Activates adenylyl cyclase resulting in generation of cAMP
-Vasculature (vasodilation of arteries and veins)
=Relax vessel wall smooth muscle
-Mast cells (anti-inflammatory)
=Inhibits release of inflammatory mediators (histamine, PGD2)
-Skeletal muscle
=Tremor
-Cell membranes
=Increased uptake of potassium
Short-acting= salbutamol
Long-acting= salmeterol

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16
Q

Describe Salbutamol

A
  • Similar drugs= terbutaline, salmeterol
  • Beta 2 adrenoceptor agonist (increase cyclic AMP), smooth muscle relaxation and bronchodilation
  • Low dose inhaled: as required or prophylactic, high dose nebulised: asthma/COPD exacerbations, other uses: hyperkalaemia
  • Tremor, tachycardia and palpitations, hypokalaemia
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17
Q

How are anticholinergics used in asthma/ COPD?

A

-Cholinergic receptors (M1,2,3) located in airways
=Acetylcholine is the neurotransmitter released from postganglionic neurones in the vagus nerve ending
-Cholinergic (muscarinic) agonists cause:
=Smooth muscle to contract so airway narrowing
=Submucosal glands to secrete mucus
-Cholinergic antagonists (anticholinergics) cause:
=Bronchodilation
=Reduced mucus production
Short-acting= ipratropium bromide
Long-acting= tiotropium

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18
Q

What are the adverse effects of anticholinergic drugs?

A 
-Reduced secretions from other glands
=dry mouth
=scratchy throat
-Reduced smooth muscle contraction
=constipation
=urinary retention
-Reduced cholinergic effect (vagal tone) on heart
=tachycardia
-Headaches
19
Q

Describe Ipratropium Bromide

A
  • Similar: tiotropium (long-acting)
  • Anticholinergic (anti-muscarinic), decreased mucus secretion, bronchodilation
  • COPD, bronchial asthma, rhinitis
  • Inhalation= tiotropium 20-40 micrograms 3-4x/day, nebulised= ipratropium 100-500 micrograms up to 4x/day
  • Dry mouth, nausea, headache
20
Q

Describe the Theophylline group

A
  • Similar: aminophylline (used IV)
  • Phosphodiesterase inhibitor- increased cAMP- PKA activation, TNFa inhibition and inhibition of leukotriene synthesis, bronchodilation
  • COPD, asthma (now rarely)
  • Twice daily slow release tablets, plasma level of 10-20 mg/L
  • Tachycardia, palpitations, nausea
  • Monitoring plasma concentration is useful (digoxin, phenytoin, gentamicin)
21
Q

What are corticosteroids?

A

Anti-inflammatory
-Inhibit inflammatory cell recruitment
-Reduce oedema by reducing permeability of vascular endothelium
-Increase anti-inflammatory mediator production (IL-1 receptor antagonist, IL-10)
-Inhibits NF-kB and AP-1 synthesis which are required for pro-inflammatory mediator production
Brown/purple inhalers

22
Q

What are the adverse effects of corticosteroids?

A

-Hyperglycaemia (careful in diabetes)
-Osteoporosis (reduced bone density)
-Proximal myopathy
-Skin thinning
-Suppression of pituitary adrenal axis
-Altered body fat distribution
-Hypertension
-Weight gain
-Growth suppression in children
-Infection susceptibility (esp. viruses, fungi)
Inhaled: beclomethasone
Oral: prednisolone
IV: hydrocortisone

23
Q

Describe Prednisolone

A
  • Similar: hydrocortisone
  • Action at nuclear receptors, immunosuppression, anti-inflammatory
  • Asthma, COPD exacerbations, RA, IBD
  • 40mg daily for several days after exacerbations, intra-articular injections may help settle a flare
  • Growth suppression, osteoporosis, weight gain, infections, skin changes, hyperglycaemia
24
Q

What are leukotrienes?

A

-Synthesised from arachidonic acid
-Production increased in allergic responses and inflammation
-Airway effects:
=Narrowing
=Increased mucus production

25
What are Leukotriene antagonists?
Montelukast -Can be used as a steroid-sparing agent -Well-tolerated but adverse effects include: =Increased infection risk =Muscle aches =Liver damage =Hypersensitivity (Vasculitis= Churg-Strauss)
26
Describe Montelukast
- Reduces airway narrowing and mucus secretion - Bronchial asthma esp. exercise induced, additive effect with inhaled corticosteroids, seasonal allergic rhinitis - 1 tablet in the evening (4mg-10mg) - Abdominal pain, thirst, headache, hyperkinesia (in children), hypersensitivity= vasculitis (Churg-Strauss)
27
Describe Cromoglicate
- Similar: Nedocromil - Stabilises mast cells and reduces release of histamine, prevents airway inflammation - Asthma prophylaxis, allergic rhinitis, conjunctivitis - Inhalation= 10mg (2 puffs) 4x/day, nebulised used in young children - Local irritation (coughing), transient bronchospasm
28
Describe oxygen therapy
- Increases alveolar oxygen concentration - Severe COPD with respiratory failure, acute asthma - Severe COPD: low concentration <28% via nasal cannula or mask, acute asthma: 15L, high flow, non re-breath mask - Respiratory depression in COPD when hypoventilation and CO2 retention is prolonged= brain adjusts= no longer sensitive to CO2 as a drive to breath/ Patients then rely on hypoxia as drive to breath may stop breathing if exposed to too much oxygen
29
What are the pros and cons of aerosol vs systemic drug delivery?
Aerosol: -Pro= delivers drug directly to required location reducing the exposure of other parts of the body -Cons: Not all drugs available (Montelukast), requires correct inhaler technique Systemic: -Pro: easy to take -Cons: greater risk of systemic side effects as all tissues exposed to same concentration as respiratory tract, slower action
30
What are the aerosol devices?
- Metered dose inhalers - Dry powder inhalers - Spacer device (spray into chamber and take several breaths) - Nasal prongs/ venture masks - Nebuliser
31
What are the pros and cons of a nebuliser?
P: Patient co-ordination not required, easy to modify dose, can give multiple medications at once C: Less portable, expensive, not all drugs soluble, requires power source
32
What are the pros and cons of a pressurised metered dose inhaler?
P: Portable, short treatments, easily reproducible doses C: difficult technique, high pharyngeal deposition, requires propellant (improved if used with spacer)
33
What are the pros and cons of a dry powder inhaler?
P: Breath-actuated, short treatment time, no propellant required C: Requires good respiratory flow, high pharyngeal deposition
34
What are the drugs that have adverse effects on the respiratory system?
``` -Drugs that cause bronchospasm =Beta-adrenoceptor antagonists (propranolol, atenolol) =NSAIDs -Drugs that suppress respiration =Opioids (morphine) =Benzodiazepines (diazepam) -Drugs that cause interstitial lung disease (fibrosis) =Amiodarone ```
35
How do NSAIDs induce bronchospasm?
Arachidonic acid released from phospholipids= precursor molecule= prostaglandins= inflammation If inhibited, more arachidonic acid down 5-Lipoxygenase pathway so more leukotrienes so more bronchoconstriction
36
What is Pneumonia?
- Infection of the gas exchange regions of the lungs - Cough, dyspnoea, pain, sputum - Sputum production, fever, inspiratory crackles, pleural rub - CXR shadowing (CT), Sputum microscopy and culture
37
What are the classifications of pneumonia?
-Community-acquired =Streptococcus pneumoniae =Haemophilus influenzae =Mycoplasma pneumoniae -Hospital-acquired (onset .48h post admission) =Gram -ve enterobacteria (E coli, salmonella) =Staph. Aureus -Aspiration =Various including anaerobes -Immunocompromised patients =Same as CAP plus pneumocystitis jiroveci
38
Describe the management of pneumonia
Antibiotics - CAP = Amoxicillin + clarithromycin - HAP= early/mild= co-amoxiclav, more severe= piperacillin/ tazobactam - Aspiration= Cefuroxime + metronidazole - Pneumocystitis jiroveci= high dose co-trimoxazole
39
Describe Amoxycillin
- Similar: Phenoxymethylpenicillin, benzylpenicillin, flucloxacillin - Bactericidal against Gram +ve cocci and bacilli - Chest infections. urinary tract infections, peptic ulcer disease (H. Pylori) - 200-500 mg three times daily oral/IV - Rash, diarrhoea, hypersensitivity
40
Describe Clarithromycin
- Similar: erythromycin - Interfere with bacterial protein synthesis - Acute bacterial exacerbations of COPD, Atypical pneumonias, allergy to penicillin - Oral: 250mg BD for 7 days or if severe 500mg BD for 14 days, IV: 500mg BD into large proximal vein - IV can cause phlebitis, multiple drug interactions (warfarin and simvastatin= macrolide antibiotic inhibits cytochrome P450 metabolism of other drugs)
41
What is Tuberculosis?
- Main pathogen in humans Mycobacterium tuberculosis - 1/3 world population have latent TB with 20% mortality - UK 10/100,000 - 50x more common if black African ethnicity than white
42
What are the risk factors of tuberculosis?
- TB contact - Live or visit TB endemic countries - Health care worker - Very young/ elderly - Immunosuppression - Malnutrition, alcoholism
43
Describe Pulmonary Tuberculosis
- Presentation site= pulmonary (60-70%), other sites= renal, lymph nodes, bone, cerebral - Chronic illness= weight loss, night sweats, cough (+/- sputum or haemoptysis) - Anorexia - General malaise
44
What is the treatment for pulmonary tuberculosis?
-Rifampicin =metabolised by liver, induces cytochrome p450 =discolours body fluids orange, rash, hepatitis, nausea, vomiting -Isonazide =metabolised by liver, enzyme inhibitor =hepatitis, rash -Pyrazinamide =metabolised by liver =hepatitis, rash, arthralgia, gout -Ethambutol =metabolised by KIDNEYS, half dose if severe CFR =retrobulbar neuritis -Pyridoxine (B6) (requires multiple drugs given over at least 6 months to kill all bacteria and avoid developing resistance)

Respiratory (41 decks)

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