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Cardiorespiratory CC > Obstructive Lung Disorder > Flashcards

Obstructive Lung Disorder Flashcards

1
Q

Male tidal volume

A

7ml/kg

About 560ml

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2
Q

Inspiratory Reserve

A

2-3L

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3
Q

Expiratory Reserve

A

1L

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4
Q

Dead space

A

Volume of respiratory tree that does not take part in gas exchange
Everything except terminal alveoli

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5
Q

Vital capacity woman

A

3-3.5L

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6
Q

Peak Flow

A

Used to monitor effectiveness of treatment

As treatment starts to work, it increases

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7
Q

Normal FEV1/FVC ratio

A

80-90%

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8
Q

Obstructive Lung Disease FEV1

A

Reduced due to narrowed airways

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9
Q

Obstructive Lung Disease FVC

A

Normal or nearly normal

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10
Q

Obstructive Lung Disease FEV1/FVC Ratio

A

Reduced

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11
Q

FEV1/FVC ratio Asthma

A

40%

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12
Q

FEV1/FVC ratio Mild obstruction

A

61-69%

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13
Q

FEV1/FVC ratio Moderate obstruction

A

45-60%

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14
Q

FEV1/FVC ratio Severe obstruction

A

<45%

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15
Q

Smoking

A

Replacement of elastin with collagen
Flow reduced
Reduces FEV1

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16
Q

Asthma essential features

A

Bronchoconstriction- airflow limitation
Hyper-secretion of mucus- clogs up airways + restricts flow more
Airway inflammation- chronic inflammation + oedema in those not managing asthma well

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17
Q

Asthma Diagnosis

A

Spirometry
Peak Flow
FEV1/FVC

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18
Q

Asthma Symptoms

A

Cough especially at night
Cough after exercise
Tightness after allergen exposure
Colds that last more than 10 days

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19
Q

Asthma signs

A 
Wheezing during normal breathing
Hyper-expansion of thorax
Increased nasal secretions
Allergic skin conditions
REDUCED PEAK EXPIRATORY FLOW
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20
Q

Peak Expiratory Flow Asthma

A

Reduced

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21
Q

Substances that Trigger Asthma

A 
Air pollutants
Pollens, mites + moulds
Animal dander
Medication
Foods
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22
Q

What causes Asthma

A

Inhaled particles act as antigens
Get trapped in mucus in airways
Bind to IgG antibodies on APCs
Stimulates CD4+ to release Interleukins 4+5
Interleukins stimulate B cells
B cells produce IgG antibody specific to antigen

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23
Q

Most common Ig

A

IgG

24
Q

First Ig to be made

A

IgM

25
Q

Ig least common in serum

A

Ig-E

Binds tightly to basophils + mast cells before interacting with antigen

26
Q

Asthma Reaction MOA

A

T Cells release extra Interleukins- IL13
Stimulates B cells to become plasma cells- make IgE as well as IgG
Ig-E attaches to mast cells
Next time that specific antigen is inhaled, mast cells release histamine + pro-inflammatory cytokines (including prostaglandin)

27
Q

Mast cell secretions cause..

A

Local inflammation- oedema
Bronchoconstriction
Mucus Secretion

28
Q

Phosphodiesterase

A

Enzyme that breaks down cyclic AMP and cyclic GMP

Needed for release of pro-inflammatory mediators

29
Q

Delayed Asthma Treatment

A

Repeated exposure- cytokines cause eosinophils + polymorphonuclear neutrophils (PMNs) to migrate into the lung tissue
Eosinophils stimulated- release enzymes that increase inflammation + epithelial damage

30
Q

Stimulated Eosinophils

A

More powerful vagally mediated reflex bronchoconstriction
Increased mucus secretion
Damage epithelial cells- less cilia- less mucus moved

31
Q

Bronchodilators

A

Beta 2 agonists
Anti-muscarinics
Phosphodiesterase inhibitors

32
Q

Anti-inflammatory Drugs

A

Steroids
Leukotriene antagonists
Anti Ig-E agonists

33
Q

Beta 2 agonists MOA

A

Mimic effect of adrenaline

Relieve acute symptoms

34
Q

Short Acting Beta 2 agonists

A

Salbutamol
Terbutaline
Bitolerol
Fenoterol

35
Q

Long Acting Beta 2 agonists (LABA)

A

Fermoterol
Bambuterol
Clenbuterol

36
Q

Anti-muscarinics MOA

A

Block parasympathetic bronchoconstriction and mucus hypersecretion
Antagonise M3 muscarinic receptors

37
Q

Anti-muscarinics examples

A

Ipratropium

Tiotropium

38
Q

Phosphodiesterase inhibitors MOA

A

Prevent formation and release of pro-inflammatory cytokines from mast cells and eosinophils

39
Q

Phosphodiesterase inhibitors

A

Theophylline

Aminophylline

40
Q

Monoclonal Antibody

A

Omalizumab
Downregulates Ig-E receptors and stabilises mast cells
Used to control severe allergic asthma that doesn’t respond to high doses of corticosteroids

41
Q

Magnesium

A

IV in emergencies
Reduces smooth muscle contractility
Antagonist to calcium

42
Q

Corticosteroids

A

Reduce bronchoconstriction, oedema + mucus formation
Stimulation of beta-2 gene expression
Suppression of expression of inflammatory genes

43
Q

Steroids

A

Help control asthma

Does not cure it

44
Q

Corticosteroids example

A

Beclomethasone
Dipropionate
Fluticasone

45
Q

Spacers

A

Improve penetration of inhaled drugs into lungs

46
Q

Nebuilsers

A

Produce inhaled mist of medication

47
Q

COPD

A

Chronic bronchitis + Emphysema combination

48
Q

Chronic Bronchitis

A

Presence of chronic productive cough without discernible cause for more than half the time over two years

49
Q

Chronic bronchitis features

A

Hypertrophy of bronchial glands
Hypersecretion
Mucous plugs
Infection/inflammation

50
Q

Chronic bronchitis cause

A

Exposure to airborne irritants

51
Q

Chronic bronchitis histology

A

Squamous cell proliferation

Massive mucous gland enlargement

52
Q

Emphysema

A

Enlargement of airspaces distal to terminal bronchioles
Destruction of lung stroma- bullae
Floppy airways- cause obstruction

53
Q

Smoking + emphysema

A

Stimulates polymorphonuclear leucocytes (PMN) to release serine elastase
Smoke inactivates elastase inhibitor alpha1-antitrypsin
Allows elastase to destroy elastic tissue of lung

54
Q

COPD + asthma similarity

A

Wheezy bronchitis

55
Q

COPD vs Asthma

A

COPD- non-reversible- actual damage to lungs

Asthma- reversible- symptoms can be reversed

56
Q

COPD + flow-volume loops

A

Same inspiration
But expiration difficult –> top of x line is scooped, but below x is normal
Expiration ends prematurely
Inspiratory capacity reduced

57
Q

Why is expiration bad in COPD

A

Expiration usually passive due to elastic recoil

Needs to be forced- much less

Cardiorespiratory CC (34 decks)

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