Physiology of Respiration Flashcards

1
Q

Where is the respiratory centre in the brain?

A

Medulla

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2
Q

Which chemoreceptors control the partial pressure of CO2 on arterial blood?

A

Medullary chemoreceptors

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3
Q

Which chemoreceptors control the partial pressure of oxygen in arterial blood?

A

Carotid body chemoreceptors

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4
Q

Which efferent pathways control airways?

A
  • Cholinergic parasympathetic nerves
  • Non-noradrenergic non-cholinergic (NANC) inhibitory nerves
    (inflammatory mediators and other bronchoconstrictors also have a role in diseased airways
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5
Q

What is FEV1 and PEFR?

A

FEV1- forced expiratory volume in 1 second

PEFR- Peak expiratory flow rate- maximal flow (l/min) after a full inhalation

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6
Q

The bronchial smooth muscle is predominantly innervated by which autonomic innervation?

A

Parasympathetic- ganglia are embedded in the walls of the bronchi and bronchioles
Postganglionic fibres innervate airway smooth muscle, vascular smooth muscle and glands

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7
Q

Types of M receptors and which type of Muscarinic receptors are pharmacologically more important?

A

M3-found on bronchial smooth muscle and glands- mediate bronchoconstriction and mucus secretion

  • M1- localised in ganglia and on postsynaptic cells and facilitate nicotinic neurotransmission
  • M2- Inhibitory autoreceptors mediating negative feedback on Ach
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8
Q

Bronchodilators released by NANC

A

VIP and Nitric oxide

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9
Q

Which parts of the lung do sympathetic nerves innervate?

A

Tracheobronchial blood vessels and glands but not human airway smooth muscle

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10
Q

Which B adrenoceptors are in the airways

A

B2- beta agonists relax bronchial smooth muscle and inhibit mediator release from mast cells- increases mucociliary clearance

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11
Q

Location and myelination factor of irritant fibres and C fibres

A

Irritant fibres- myelinated- Upper airways

C fibres- unmyelinated- low airways

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12
Q

Which tachykinins are released with the excitation of sensory nerves?

A

Substance P and neurokinin A

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13
Q

Name two drugs used to treat other conditions which affect the lung and can cause fibrosis

A
Amiodarone- class III antiarrhythmic drug- potassium channel blocker
Methotrexate- chemotherapy agent and immunosuppressant
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14
Q

What is asthma?

A

It is an inflammatory condition in which there is recurrent reversible airway obstruction in response to irritant stimuli that are too weak to effect non-asthmatic subjects- causes wheezes and needs treatment

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15
Q

Characteristics of asthma

A
  • Inflammation of the airway
  • Bronchial hyperreactivity
  • reversible airways obstruction
    Intermittent attacks of wheezing, shortness of breath and sometimes cough
    Acute asthma causes hypoxaemia
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16
Q

Pathogenesis of asthma

A

Exposure of genetically disposed individuals to allergens: activation of Th2 lymphocytes and cytokine generation promotes:
- differentiation and activation of eosinophils
IgE production and release
- Expression of IgE receptors on mast cells and eosinophils

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17
Q

Characteristics of the immediate phase of an asthma attack

A

Abrupt

  • spasm of the bronchial smooth muscle
  • allergen interaction with mast cell-fixed IgE causes release of histamine, leukotriene B4 and Prostaglandin D2.
18
Q

Characteristics of the late phase

A

Late phase or delayed response and may be nocturnal.

Progressing inflammatory reaction, initiation, of which occurred during the first phase, influx of Th2 lymphocytes

19
Q

Two categories of antiasthma drugs

A

Bronchodilators and anti-inflammatory agents

20
Q

5 steps of treatment

A

1- mild - salbutamol
2- add ICS
3- uncontrolled add LABA- salmeterol or formoterol- minimises the need for increased doses of inhaled corticosteroid
4- Theophylline and leukotriene antagonists- montelukast- coticosteroid sparring effect
5- prednisolone in addition to oral corticosteroid

21
Q

Bronchodilators other than B2- adrenoceptor agonists

A

Theophylline, cysteiny leukotriene receptor antagonists and muscarinic receptor antagonists

22
Q

How are B2 adrenoceptor agonists usually given

A

Inhalation of aerosol, powder or nebulised solution

23
Q

SABA and LABA examples

A

SABA- Salbutamol - inhalation- max effect within 30 min and duration of action 3-5h

LABA- Salmeterol and formoterol- inhalation- duration of action is 8-12 hours

24
Q

Theophylline characteristics

A
  • Methylxanthine
  • Inhibits phosphodiesterase and blocks adenosine receptors
  • Narrow therapeutic window
  • Antibiotics increase half-life, anti-convulsants
25
Q

Which drugs are third line for asthma?

A

Cysteinyl leukotriene receptor antagonists

26
Q

Commonest adverse effect of B2 adrenoceptor agonist

A

Tremor- tachycardia and cardiac arrhythmias

27
Q

Unwanted side effects of Theophyllines

A

Insomnia, nervousness, seizures - it has a very narrow therapeutic index

28
Q

Main SAMA

A

Ipratropium bromide- quaternary derivative of atropine

29
Q

Route of administration of ipratropium?

A

Aerosol inhalation

30min after inhalation- max effect can be felt

30
Q

Main LAMA used

A

Tiotropium

31
Q

TWO LTRAs

A

Montelukast, zafirlukast

32
Q

Which drugs are used for anti-inflammatory action in asthma?

A

Glucocorticoids

33
Q

MOA of glucocorticoids

A

Restrain clonal proliferation of Th cells- reduce transcription of gene for IL2 and decrease formation of cytokines (Th2 cytokines that recruit and activate eosinophils and are responsible for production fo IGE)

34
Q

Main compounds of corticosteroids used

A

Beclomethazone, budesonice, fluticasone (potent), mometasone, ciclesonide- given by inhalation with metered dose or dry powder inhaler

35
Q

Example of higher potency glucocorticoids

A

Budesonise and fluticasone

36
Q

Glucocorticoids given to patients who have acute exacerbations of asthma

A

Oral prednisolone and IV hydrocortisone

37
Q

Treatment for acute asthma

A
  • Oxygen >/ 60%
  • Inhalation of nebulised salbutamol
  • IV hydrocortisone followed by oral prednisolone
  • IV magnesium 1.2-2mg for 20 mins
  • IV theophyliine
38
Q

COPD clinical features

A

PROGRESSIVE BREATHLESSNESS
cough- becomes chronic
Pulmonary hypertension- late feature

39
Q

Pathogenesis of COPD

A
  • Fibrosis of small airways
  • Obstruction/destruction of alveoli and elastin fibres
  • Emphysema causes resp failure- destroys alveoli- impairs gas transfer
40
Q

Treatment of COPD

A
Stop smoking 
LABA- modest benefit
Combat mucous hypersecretion 
Look at chest disease lecture
LABA and LAMA+ ICS