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RESP > Asthma > Flashcards

Asthma Flashcards

1
Q

What is asthma?

A
  • An inflammatory disease of lung airways
  • reversible airway obstruction
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2
Q

What is asthma characterized by?

A
  • Narrowed airways; ↓ gas exchange
  • Inflammation of airways with inflammatory cells
  • Bronchoconstriction + bronchospasm
  • Mucus production
  • cholinergic nerve over-activity
  • smooth muscle hypertrophy
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3
Q

What factors contribute to allergic asthma?

eosinophilic

A
  • Allergens (most common)
  • Occupational (industrial chemicals)
  • Air pollutants
  • Infections (RSV, influenza)
  • Exercise
  • Medicines (aspirin, B-blockers)
  • Stress
  • Genes
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4
Q

What factors contribute to non-allergic asthma?

non-eosinophilic

A
  • Adults
  • Nasal polyps
  • Drug hypersensitivity; aspirin, penicillin
  • COPD
  • poor prognosis

does not respond to corticosteroids

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5
Q

What tests are done for asthma?

A
  • Family history
  • Physical exam
  • Spirometry
  • Bronchodilator reversibility test
  • Allergy test

in more sever cases CT scan

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6
Q

What happens to bronchioles during SNS?

A
  • Bronchodilation
  • Adrenaline activates β2 receptors
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7
Q

What happens to bronchioles during PNS?

A
  • Bronchoconstriction
  • Ach binds to M3 receptors
  • increased mucus secretion
  • vagus nerve

Muscarinic M3

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8
Q

What are the types of bronchodilators?

A
  • β2 agonists
  • Muscarinic antagonists/Anti-cholinergic
  • Methylxanthines

SNS activation, PNS inactivation

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9
Q

What are SABAs?

Short acting Beta agonists

A
  • Salbutamol
  • Terbutaline
  • acute asthma attacks + exercise relief
  • short term relief for COPD
  • last 4-6 hrs
  • bind directly to orthosteric B2 receptor sites
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10
Q

What are LABAs?

Long acting beta agonists

A
  • Salmeterol / Formoterol / Indacaterol / Vilanterol
  • used for clients with more frequent attacks with corticosteroids
  • last 12-24 hrs
  • bind to orthosteric and exo-sites for prolonged receptor activation
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11
Q

What are the contraindications of beta-blockers?

A
  • can precipitate asthma
  • Non-selective BB: cause bronchoconstriction
  • Cardioselective: safer but still risky

non-selective targets B1 + B2, cardioselective target B1 only

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12
Q

What are some side effects of B-agonists?

A
  • hypersensitivity to drug
  • hypertension
  • tremors
  • muscle cramps
  • thyroid disease
  • DM
  • tachyarrhythmias
  • CAD
  • seizures
  • hypokalaemia
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13
Q

What is the MOA of B2 agonists?

A
  • Bind to B2 adrenoreceptors
  • Increase cAMP via G-protein linked activation of AC
  • Bronchodilation of smooth muscle
  • inhibit mediator release from mast cells
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14
Q

What are Muscarinic receptor antagonists?

A

Ipratropium (the only SAMA)
- antagonist for M1, M2, M3
- bronchodilator
- reduces mucous secretion
- slower acting that B2 agonist

Tiotropium (LAMA)
- inverse agonist for M1,M3

can be ipratropium/tiotropium bromide

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15
Q

What are side effects of Muscarinic receptor antagonists?

A
  • usually well tolerated
  • dry mouth and urinary retention
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16
Q

What are methylxanthines?

A
  • have immunomodulatory effects
  • found in tea, coffee, cocoa
  • Caffeine, Theophylline, Aminophylline
17
Q

What is the MOA of methylxanthines?

A
  • bronchodilation
  • inhibit phosphodiesterase
  • more cAMP, cGMP
  • anti-inflammatory actions
  • improves diaphragm strength
18
Q

Give information about theophylline

A
  • most common xanthine drug
  • taken orally
  • low TI
  • drugs interact with theophylline, affecting its metabolism with CYP1A2
  • macrolides inhibit CYP1A2, ↑ toxicity of theo
  • smoking + caffeine also effect theo
  • rifampicin increases CYP1A2, ↓ theo

aminophylline taken by IV - ICU, macrolides: clarithromycin, erythromycn

19
Q

What are side effects of methylxanthines?

A

low TI, so SE with high concentrations:
- nausea
- arrhythmias
- tremor, seizure

TI = therapeutic index

20
Q

Where are methylxanthines metabolised?

A
  • liver
  • Cytochrome P450; CYP1A2
21
Q

Explain the pathophysiology of asthma?

A
  1. Initial phase: interaction of allergen with mast cell IgE, release of histamine + PGD2 - bronchoconstriction
  2. Intermediate phase: chemokine release - IL4, IL5 and IL13, leukocyte release
    Mucosal oedema
  3. Late phase: Influx of Th2 cells, neutrophils and eosinophils activated - TNF-a, IFN-y released
    Lung epithelial damage
22
Q

What anti-inflammatory drugs are used in asthma treatment?

A
  • Glucocorticoids
  • Cromones
  • Leukotriene synthesis inhibitors
  • Leukotriene receptor antagonists
23
Q

What are corticosteroids?

A
  • Beclomethasone (inhaled)
  • Prednisone (oral)
  • Hydrocortisone (IV)
24
Q

What are side effects of inhaled corticosteroids?

A
  • Oral candidiasis (thrush)
  • Dysphonia (myopathy of laryngeal muscles)
25
Q

What are systemic side effects of oral corticosteroids?

A
  • adrenal suppression
  • infections
  • hypertension, fluid retention
  • osteoporosis, myopathy, obesity, growth stunting, catarcts, glaucoma
  • glucose intolerance
26
Q

What do we give first in an acute asthma attack?

A

Bronchodilators FIRST, then corticosteroids

27
Q

How do anti-leukotrienes work?

A
  • most effective in exercise induced bronchioconstriction
  • not for acute attacks
  • low s/e
  • orally

Leukotriene receptor antagonism:
- blocks cysteinyl leukotriene type 1 receptors

Leukotriene synthesis inhibition:
- Inhibitis 5-lipooxygenase enyzme, stops formation of leukotriene

28
Q

How do glucocorticoids work?

as anti-leukotriene

A
  • inhibit arachadonic acid synthesis
  • suppresses phospolipase A2
29
Q

What are cromones?

A
  • mast cell stabilisers
  • sodium cromogylate + nedocromil
  • inhibit dengranulation and reduce mediator release
  • inhibit eosinophil accumulation
  • inhaled

blocks release of histamine, chemokines and leukotrienes from mast cells

30
Q

What are some newer anti-inflammatory approaches for asthma?

A
  • Omalizumab; Anti-IgE
  • methotrexate
  • gold
  • cyclosporin
  • anti-TNF-a agents
31
Q

How is acute asthma managed?

A
  1. SABA: salbutamol
  2. Muscarinic antagonist: ipratropium (inhaled)
  3. Corticosteroid: prednisolone (oral)
  4. hospitalization

Magnesium sulphate in IV used for life threatening situations

32
Q

How is chronic asthma managed?

A
  1. give SABA as reliever (optional)
  2. low does ICS for controller
  3. leukotrine modifier
  4. methylxanthine: theophylline
  5. LAMA

from 2 onwards switch SABA to LABA and increase ICS dose as needed

33
Q

What are the microscopic features of asthma?

A
  • neutrophils + eosinophils
  • mast cell degranulation
  • basement membrane thick
  • lumen filled with mucus
  • hypertrophy of smooth muscle + goblet cells
34
Q

What are the cardinal symptoms of asthma?

A
  • Cough (nocturnal)
  • Wheeze
  • SOB
  • usually onset in childhood
  • rhinitis and eczema
35
Q

What is the classic triad in asthma?

A
  • Dyspnoea
  • Wheeze
  • Cough (non-productive)

no sputum in cough

36
Q

What are the cardinal signs of asthma?

A
  • wheezing upon auscultation
  • reduced PEFR
  • reduced FEV1
  • accessory muscle use
  • cyanosis
  • hyperinflation of chest
37
Q

Why are asthma symptoms worse during the night and in the morning?

A
  • cortisol ↓ 12am
  • adrenaline ↓ 4am
  • nocturnal symptoms 2-3am onwards

RESP (20 decks)

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