Respiratory Flashcards

0
Q

What is seretide?

A

Preventer product containing fluticasone (glucocorticoid) and salmeterol (long acting beta 2 agonist)

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1
Q

Asthma

A

Yourface

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2
Q

Pseudoephidrine mechanism of action

A

1) enters noradrenergic nerve and is taken up into storage vesicles in exchange for NA.
2) NA acts on post synaptic membrane and acts on alpha 1 receptors - causes vasoconstriction therefore decreased odema and fluid leakage.

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3
Q

Name two short acting beta agonsists

A

Salbutamol

Terbutaline

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4
Q

Name two long acting beta agonists

A

Salmeterol

Formoterol

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5
Q

Name two examples of M receptor antagonists

A

Ipratropium

Tiotropium

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6
Q

Three examples of inhaled glucocorticoids

A

Budesonide
Fluticasone propionate
Beclomethasone Dipropionate

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7
Q

Two examples of oral glucocorticoids

A

Prednisolone

Hydrocortisone

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8
Q

Mechanism of action of Beta-2 adrenoreceptor agonist

A

Binds to GPCR Beta-2 adrenoreceptors on lining of airways.
Activates Gs pathway -> increased adenylate cyclase activation -> PKA activation -> decrease intracellular Ca ions + dephosphorylation of MLCK -> decreased excitability of cells -> BRONCHODILATION

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9
Q

Mechanism of action of Glucocorticosteroids

A

Bind to GRalpha receptor (homodimerized complex) in cytoplasm. This complex moves into nucleus.
Transactivation:
- complex binds to positive GRE within promoter -> upregulates transcription of anti-inflammatories
Transrepression:
- complex binds to negative GRE -> displaces bound transcription factors -> reduce transcription of pro-inflammatories

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10
Q

What is the difference between SABA and LABA

A
Short acting beta agonists:
- effective in minutes
- 3-5 hr duration
- reliever medication for attacks
Long acting beta agonists
- effective in 10-20 minutes
- 8-12 hr duration
- symptom control/preventer
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11
Q

Mechanism of action of M receptor antagonists

A

Prevent binding of ACh -> prevent activation of Galphaq pathway -> decrease PLC -> decrease IP3 -> decrease intracellular Ca ions -> dephosphorylation of MLCK -> muscle relaxation

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12
Q

Mechanism of action of Pseudoephedrine

A
  • Enters cytoplasm of noradrenergic nerve terminals via Uptake 1 transporter
  • Taken up into vesicles via VMAT in exchange for noradrenaline (NA) into the cytoplasm
  • Some NA degraded by MAO enzyme, the rest exits nerve terminal via Uptake 1 in exchange for pseudo
  • Pseudo also inhibit NA reuptake
  • In the synapse, NA acts on postsynaptic receptors to cause vasoconstriction
  • Pseudo is resistant to MAO breakdown
  • It is used to treat non-allergic rhinitis
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13
Q

Mechanism of action of Antihistamines

A

Reversible competitive antagonism of histamine at H1 receptors

  • decrease vascular permeability
  • decrease pruritus
  • relaxation of smooth muscle in resp and GI tract

-They are used to treat allergic rhinitis

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14
Q

What makes an antihistamine non-sedating?

A

Decreased lipophilicity -> less able to cross BBB -> less CNS side effects

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15
Q

Examples of non-sedating oral antihistamines

A

Fexofenadine
Cetirizine and Levocetirizine
Loratadine and Desloratadine

16
Q

Examples of sedating oral antihistamines

A
Azatadine
Pheniramine
Chlorpheniramine
Dexchlorpheniramine
Cyproheptadine
Promethazine
17
Q

Mechanism of action of intranasal anticholinergics

A

.

18
Q

Mechanism of action of Mast cell stabilisers

A

reduces hyperreactivity and reduces immediate & delayed phases of asthma

19
Q

Under what cirumstances would you refer patient to doctor?

A
  • White or yellow spots on a bright red throat
  • Swollen tonsils or lymph nodes
  • Pain when swallowing
  • Fever (over 38.3 degrees)
  • Sudden, severe sore throat
  • Difficulty breathing
  • Dysphagia
  • Persistant sore throat
  • Persistant thrush
20
Q

Expectorant examples

A

expectorants improve the ability to expectorate mucosal secretions

  • hydration with steam
  • Gauiphenesin (decreases viscosity of phlegm)
  • Ammonium Chloride (avaliable as “Senega & Ammonia mixture. Irritates bronchial mucoasa causing increased mucosal fluid)
21
Q

Mucolytic examples

A

Mucolytics break down mucus

  • bromhexine (break disulfide bonds between gel-forming mucins & therefore decreases viscosity)
  • acetylcysteine (breaks disulfide bonds like bromhexine. Used in cystic fibrosis)
22
Q

Centrally acting cough suppressants

A

Depress cough centre in medulla (NTS)
Narcotic
- codiene, dihydrocodeine, pholcodine
- activate opioid receptors –> results in less glutamate & NMDA activation (receptor that causes cough)
Non-Narcotic
- dextromethorphan (NMDA receptor antagonist/sigma agonist)
- diphenhydramine - antihistamine/TRPV1 antagonist

23
Q

Peripherally acting cough suppressants

A
  • Local analgesic effect or anti-inflammatory effect
    - camphor, menthol
    - benxydamine (difflam throat spray)
  • Enhance drainage of bronchial secretions by reducing viscosity (expectorants)
  • relaxation of bronchial smooth muscle (bronchodilators)
  • demulcent or soothing effect on irritated throat & airways (honey, syrup, thickener, expectorants)
24
Q

Decongestants

A
  • oxymetazoline (spray)
  • xylometaxoline (spray)
  • pseudoephedrine (oral)
  • phenylephrine (oral)
25
Q

Rhinitis Treatments

A

1) decongestants
2) antihistamine
3) leukotriene Receptor antagonist
4) Corticosteroids
5) Mast cell stabilisers
6) Intranasal anticholinergics

26
Q

Drugs that can be used to treat asthma during pregnancy & breastfeeding

A
  • bronchodilators - salbutamol, tebutaline
  • glucotorticoids - budesonide
  • avoid long acting beta 2 agonists during first trimester (unless already on LABA –> don’t stop)
27
Q

When are leukotriene antagonists used? Give an example

A

3rd line use treatment in asthma

eg. montelukast