PHARM Asthma & COPD - Week 2 Flashcards

(37 cards)

1
Q

Asthma pathology

A

Increased smooth muscle, build up of mucous, BM thickening.

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2
Q

Symptoms of asthma

A
  • Recurring episodes of breathing problems.
  • Shortness of breath.
  • Wheezing/chest tightness
  • Night-time or early morning coughing.
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3
Q

2 x types of asthma

A
  • Extrinsic – allergic/T2 type (most common)
    o Involves IgE antibodies/mast cell & basophilic degranulation
    o Triggered by re-exposure to allergens (e.g., pollen, house dust mites, pets).
  • Intrinsic – non-allergic/non-specific (more severe)
    o Hyper-responsive airways
    o ‘Non-specific bronchial hyperreactivity’
    o Triggered by exercise, cold, infection.
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4
Q

What immune cells are responsible for driving 2 types of asthma?

A

T2/allergic/extrinsic asthma - high eosinophils
Non-T2/non-allergic/non-specific/intrinsic asthma - high neutrophils

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5
Q

SABA expand. Drug type examples.

A

Short acting B2 agonist. Salbutamol/albuterol (ventolin/asmol).

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6
Q

SABA administration.

A

Inhalation.

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7
Q

What do SABAs protect against?

A

Exercise-induced asthma.

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8
Q

MOA SABAs

A
  • MOA: mimick effect of adrenaline with selective action on B2 adrenoreceptors -> adenylcyclase -> c35AMP -> muscle relaxation/bronchodilation
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9
Q

SABA onset

A

5-15min

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10
Q

SABA duration of action

A

3-6hrs

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11
Q

SABA adverse effects

A
  • Adverse effects: tachycardia, muscle tremor, receptor downreglation/desensitisation decreases efficacy in cases of overuse, infection, smoking, underlying inflammation left untreated.
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12
Q

LABA expand. Drug examples.

A

Long acting B2 adrenoreceptor agonist. Formoterol.

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13
Q

LABA administration.

A

Inhalation.

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14
Q

What do LABA & ICS protect against?

A

T2-type asthma (w eosinophilic response)

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15
Q

When should LABA & ICS be used?

A

Short term exacerbation OR for severe asthma unresponsive to other therapies.

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16
Q

LABA & ICS MOA

A
  • MOA : steroids must enter cytoplasm of target cells -> acts on receptor -> translocates to nucleus -> regulating gene expression -> promote anti-inflammatory protein synthesis -> bind to pro-inflammatory transcription factors (e.g., NFkB) to downregulate inflammatory factors
17
Q

LABA & ICS adverse effects

A
  • Adverse effects: suppress endogenous glucocorticoid synthesis, Cushing’s syndrome, suppress infection & injury response, behavioural disturbances, cataracts, glaucoma, metabolic effects, growth suppression, poor delivery can cause dysphonia & oral thrush.
18
Q

Omalizumab target. Recommended for which group of pts.

A
  • Omalizumab – recombinant mAb against IgE (use restricted to severe, persistent allergic asthma uncontrolled even with high doses of corticosteroids).
19
Q

Mepolizumab target. Recommended for which group of pts.

A
  • Mepolizumab – recombinant mAb against IL-5 (use restricted to severe eosinophilic asthma in adults only).
20
Q

Dupilumab target. Recommended for which group of pts.

A
  • Dupilumab – recombinant mAb against IL-4/IL-3 receptor (use restricted to adults with severe allergic asthma).
21
Q

Symptoms of COPD

A
  • Shortness of breath
  • Wheezing
  • Coughing
  • Increased mucous production
  • Recurrent chest infections
  • Muscle wasting.
22
Q

Potential causes of COPD

A
  • Smoking
  • Frequent lung infections as a child
  • Indoor smoke (e.g., wood, coal, cow dungs, crop residues)
  • Occupational dust @ chemical exposure
  • Genetic reasons (a-1 antitrypsin deficiency)
23
Q

What can a1 antitrypsin deficiency lead to? How?

A

Early onset emphysema. Lungs lack a1 antitrypsin coating - leaving them open to damage by neutrophil elastase. Liver damage also occurs due to trapped a1 antitrypsin present here.

24
Q

Signs & symptoms of chronic bronchitis.

A

Remember blue bloater & pink puffer.
Overweight, cyanosis, elevated Hb, peripheral oedema, wheezing, chronic daily productive cough.

25
Signs & symptoms of emphysema.
Remember blue bloater & pink puffer. Older & thinner, severe dyspnoea, quiet chest, CXRT revealing hyperinflation w flattened diaphragms & permanent enlargement & destruction of airspaces distal to the terminal bronchiole.
26
What immune cells are responsible for driving COPD?
Neutrophils.
27
SAMA expand. Drug examples.
Short acting M3 antagonist. Ipatropium/tiotropium.
28
SAMA adverse effects.
* Adverse effects: inhibit salivation -> dry mouth, blurred vision, urinary retention.
29
SAMA effect.
* Protect against increased parasympathetic drive by decreasing airway muscle contraction & mucous production.
30
When are ICS used to treat pts w COPD?
In pts who have eosinophilic elevation.
31
When are short term oral steroids usually used in pts w COPD?
Recovery from COPD exacerbations.
32
Issues with steroid use in pts w COPD?
Suppressed immunes system -> increased risk of pneumonia.
33
Therapy for pts w a1-antitrypsin deficiency
Replacement therapy (derived from human plasma).
34
Step wise treatment for asthma. Examples of common medications prescribed.
ICS-LABA/ICS-SABA as needed, regular, low-dose ICS-LABA/ICS-SABA, medium-dose, regular ICS-LABA, add LAMA (consider high-dose, regular ICS-LABA OR anti-IgE, anti-IL5...). LABA e.g., formoterol/symbicort. ICS e.g., budesonide. SABA e.g., salbutamol/ventolin.
35
Step wise treatment for COPD.
SABA or SAMA as needed, SABA or SAMA w LABA or LAMA, previous w ICS, LABA & LAMA & ICS recently approved, previous (consider anti-inflammatory agents).
36
What drug classes are typically considered relievers? Preventers?
SABA/SAMA. LABA/LAMA/ICS.
37
Why are SABAs preferred over SAMAs for asthma treatment?
SABAs preferred for asthma compared to SAMAs - as SABAs target all leukotrienes, histamines... whereas SAMAs only target ACh mediator.