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Asthma RCM week 1 > Asthma: diagnosis, monitoring, pathophysiology, and management > Flashcards

Asthma: diagnosis, monitoring, pathophysiology, and management Flashcards

1
Q

What is asthma defined by

A

Reversible increases in airway resistance, involving bronco constriction and inflammation

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2
Q

What is asthma characterized by

A

Reversible decreases in the FEV1:FVC (less than 70-80% suggests increases airway resistance)

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3
Q

What is FEV1

A

Amount of air a person can force out of their lungs in 1 second

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4
Q

What is FVC

A

Forced vital capacity (total amount of air exhaled)

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5
Q

How can you also see if a person has asthma (another diagnostic test)

A

Measure their PEF (peak expiratory flow)

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6
Q

What is the PEF like in an asthma patient

A

Variable- which is improved with a Beta2 agonist

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7
Q

What is PEF

A

Maximum velocity of a person’s expired air (peak expiratory flow)

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8
Q

What is COPD

A

Chronic obstructive pulmonary disease

-chronic bronchitis+ emphysema

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9
Q

What is chronic bronchitis

A

Increased mucus, airway obstruction, intercurrent infections

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10
Q

What is emphysema

A

Destruction alveoli

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11
Q

What is the FEv1 like in a person with COPD

A

Reduced

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12
Q

What is the PEF like in a person with COPD

A

Little variation

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13
Q

What is chronic bronchitis and emphysema mostly caused by

A

90% caused by smoking

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14
Q

Which nervous system is used to relax airways

A

Sympathetic

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15
Q

How does the sympathetic nervous system relax the airways

A

Release of circulating adrenaline acting on beta2-adrenoreceptors on bronchial smooth muscle and activates them to cause relaxation (bronchodilation)

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16
Q

How does parasympathetic nervous system cause the constriction of airways

A
  • vagus nerve releases acetylcholine at the ganglia

- Binds to muscarinic receptors which activates it and causes constriction

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17
Q

How else is acetylcholine released to cause muscle constriction

A

End organ of tissue

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18
Q

How else does sympathetic nervous system control bronchial calibre

A

Sympathetic fibers release NA which acts on adrenoreceptots on parasympathetic ganglia to inhibit transmission

-Beta2 adrenoceptors also are on mucus glands to inhibit secretion

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19
Q

What nerves do airways have

A

sensory nerves

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20
Q

What happens if dust gets in airway

A

Stimulates sensory nerve, which then causes bronchoconstriction (reflex response locally) (cough reflex)

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21
Q

What are asthmatic attacks genetically provoked by

A
  • allergens
  • cold air
  • viral infections
  • smoking
  • exercise
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22
Q

What are the phases of an asthma attack

A

-May be characterized by Early phase followed by Late phase (which is more inflammatory)

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23
Q

Clinical features of asthma

A

-wheezing
-breathlessness
-tight chest
-cough (worse at night/exercise)
(nocturnal in children)
-Decreases in FEV1, reversed by a Beta2 agonist

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24
Q

Once a stimulus is detected, what happens in lungs

A

-mast cells, mononuclear cells, release mediators

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25
Q

What are the mediators that the mast cells and mononuclear cells release

A

Spasmogens (immediate response) which constrict the airways and cause bronchospasm

Chemotaxins (signals to white blood cells which tell them to go to the lungs and cause the Late phase (inflammation)

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26
Q

Examples of spasmogens

A

Histimine
Prostaglandin D2
Leukotrienes C4 and D4
Platelet activating factor (PAF)

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27
Q

How are prostaglandins Made

A

In the cell membranes, we all have arachidonic acid. Via the COX pathway, it is metabolized to prostaglandin

28
Q

What is the role of prostaglandin

A

Bronchoconstrictor

29
Q

How are leukotrienes made

A

Arachidonic acid goes down the LOX pathway to form leukotrienes

30
Q

What are leukotrienes used for

A

Spasmogens, and are also inflammatory

31
Q

What is histamine released by

A

Mast cells

32
Q

Examples of chemotaxins and their role

A
  • Leukotriene B4, PAF
  • leads to Late Phase
  • Attract leukocytes, especially eosinophils and mononuclear cells
  • Leads to inflammation and airway hyper-reactivity
33
Q

What do bronchodilator reverse and what phase is this

A

Bronchospasm (early phase)

34
Q

What kind of relief do bronchodilators provide

A

Rapid relief

35
Q

What other drugs can be used and what is this used for

A

-preventers used to prevent an attack

36
Q

What is the drug used as a Beta2 adrenoceptor agonist

A

Salbutamol

37
Q

When is salbutamol used

A

Agent of first choice

38
Q

What does salbutamol do

A

Increases FEV1

  • Binds to Beta 2 adrenoceptors on smooth muscle
  • Produced G protein
  • This G proteins activates Adenylylcyclase which is an enzyme which leads to the production of cAMP (second messenger) which causes muscle relaxation
39
Q

What is cAMP broken down into

A

PDE into AMP

-stops action of cAMP

40
Q

Long term effect of beta2 agonist

A

Leads to the lessened responsiveness of the beta2 adrenoceptors which makes the drug less effective

41
Q

What drugs are used as a preventative measure and for long term control

A

Long acting beta agonists (LABA)

42
Q

Example of a LABA

A

Salmetarol

43
Q

What does salmetarol do

A

Dilate the airways for 12 hours so is used for long term control overnight

44
Q

What are the two theories of action of xanthines

A
  • Adenosine receptor antagonists

- Phosphodiesterase inhibitors

45
Q

The are xanthines used

A

In an emergency (intravenous insertion in an emergency)

46
Q

What do xanthines do when inhabiting phosphodiesterase inhibitors

A

Xanthines PDE which means that the breakdown of cAMP is inhibited and so the action of cAMP is prolonged and so theres more muscle relaxation by the action of salbutamol

47
Q

What are muscarinic M-receptor antagonists mostly used in

A

COPD (limited value in asthma)

48
Q

What do muscarinic M-receptor antagonists do

A

Block parasympathetic bronchoconstriction

49
Q

Example of muscarinic M-antgonists

A

Tiotropium

50
Q

Side effects of muscarinic M-antagonists

A
  • Dry mouth
  • constipation
  • Blurred vision

because you’re blocking parasympathetic nervousb system

51
Q

How to reduce musarinicM- antagonist side effects

A

Inhale the drug

52
Q

What are anti-inflammatory agents used as

A

Preventative measure

THEY DO NOT REVERSE AN ATTACK

53
Q

Drug name used as an anti-inflammatory agent

A

Corticosteroids

-eg beclometasone (brown inhaler)

54
Q

What do corticosteroids do

A

1) Go into the cell because its lipid soluble
2) Activate intracellular receptors
3) Intracellular-drug complex goes to nucleus
4) Tells nucleus which bits of DNA to produce mRNA for
5) mRNA comes out of the nucleus and codes for protein Lipocortin/Annexin A1
6) Lipocortin/annexin A1 inhibits phospholipase A2 which is used to synthesize arachidonic acid (which produces leukotrienes and prostaglandins which inflame the airways)

55
Q

What are steroids given with and why

A

Beta 2 agonists to reduce the receptor down-regulation

56
Q

Side effects of steroids taken

  • orally
  • Inhaled (and how to prevent this)
A

Orally- Adrenal suppression

Inhalation- Throat infections, hoarseness (so wash mouth out afterwards)

57
Q

What is salmetarol

A

Beta 2 agonist

58
Q

What are leukotriene receptor agonists (LTRAs) used for

A

Block the action of leukotrienes

-preventative and bronchodilators

59
Q

Example of a leukotriene receptor antagonist drug

A

Montelukast

60
Q

Initial line of treatment for an asthma patient

A

Short acting Beta2 agonist (salbutamol) plus a regular inhaled steroid (beclametasone)

61
Q

If patient’s asthma is not sufficiently controlled by first line of treatment, what do you use next

-and if this fails?

A

Trial of LABA (or LTRA or xanthine if this fails)

-Increase dose of inhaled steroid

62
Q

If the patients asthma is not controlled by increasing dose of inhaled steroid?

A

Add oral steroid

63
Q

How to know whether to go to next line of treatment

A

If salbutamol is used >2 times a week

64
Q

When is a spacer device used (the bottle)

A
  • In patients with poor technique

- Reduce steroid impaction

65
Q

What should you use before a steroid and what to do after steroids

A

Bronchodilator

-wash mouth out

Asthma RCM week 1 (12 decks)

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