Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiratory > Drugs affecting the respiratory system > Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the symptoms of asthma?

A
  • Breathlessness (chest tightness)
  • Wheeze
  • Cough
  • Diurnal variability (worse in the morning or at night)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the provoking factors of asthma?

A
  • Exercise/ hyperventilation
  • Food, additives
  • Drugs (NSAIDs, beta-blockers)
  • Cigarette smoke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the non-pulmonary complications of COPD?

A
  • Right heart failure (cor pulmonale)
  • Peripheral oedema
  • Weight loss
  • Muscle wasting
  • Osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are COPD risk factors?

A
  • Smoking
  • Occupation
  • Recurrent infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the signs of COPD?

A
  • Resting RR> 20 breaths/min
  • Accessory muscles
  • Pursed lipped breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What are Leukotriene antagonists?

A

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
Q

Describe Montelukast

A
  • 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
Q

Describe Cromoglicate

A
  • 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
Q

Describe oxygen therapy

A
  • 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
Q

What are the pros and cons of aerosol vs systemic drug delivery?

A

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
Q

What are the aerosol devices?

A
  • Metered dose inhalers
  • Dry powder inhalers
  • Spacer device (spray into chamber and take several breaths)
  • Nasal prongs/ venture masks
  • Nebuliser
31
Q

What are the pros and cons of a nebuliser?

A

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
Q

What are the pros and cons of a pressurised metered dose inhaler?

A

P: Portable, short treatments, easily reproducible doses
C: difficult technique, high pharyngeal deposition, requires propellant (improved if used with spacer)

33
Q

What are the pros and cons of a dry powder inhaler?

A

P: Breath-actuated, short treatment time, no propellant required
C: Requires good respiratory flow, high pharyngeal deposition

34
Q

What are the drugs that have adverse effects on the respiratory system?

A 
-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
Q

How do NSAIDs induce bronchospasm?

A

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
Q

What is Pneumonia?

A
  • 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
Q

What are the classifications of pneumonia?

A

-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
Q

Describe the management of pneumonia

A

Antibiotics

  • CAP = Amoxicillin + clarithromycin
  • HAP= early/mild= co-amoxiclav, more severe= piperacillin/ tazobactam
  • Aspiration= Cefuroxime + metronidazole
  • Pneumocystitis jiroveci= high dose co-trimoxazole
39
Q

Describe Amoxycillin

A
  • 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
Q

Describe Clarithromycin

A
  • 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
Q

What is Tuberculosis?

A
  • 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
Q

What are the risk factors of tuberculosis?

A
  • TB contact
  • Live or visit TB endemic countries
  • Health care worker
  • Very young/ elderly
  • Immunosuppression
  • Malnutrition, alcoholism
43
Q

Describe Pulmonary Tuberculosis

A
  • 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
Q

What is the treatment for pulmonary tuberculosis?

A

-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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions