Respiratory Medicine: Asthma and COPD - PowerPoint Presentation

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Respiratory Medicine:Asthma and COPD

Dr Rickbir Singh Randhawa

FY1

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Definition:Asthma

Chronic inflammatory airway disease characterised by

reversible airway obstruction

, airway hyper-responsiveness and bronchial inflammation.

Three factors contribute to reversible airway narrowing:

1. Bronchial smooth muscle contraction triggered by a variety of stimuli

2. Mucosal swelling/inflammation caused by mast cell and basophil degranulation- release of inflammatory mediators

3. Increased mucus production

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Definition:COPD

Chronic progressive lung disorder characterized by

airway obstruction with little or no reversibility.

It includes the following:

Emphysema:

defined histologically as permanent destructive enlargement of air spaces distal to the terminal bronchioles

Chronic Bronchitis:

defined clinically as a chronic cough with sputum production on most days for 3 months per year over 2 successive years.

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AetiologyAsthma

Genetic factors-

+VE family Hx, atopic (eczema, allergic rhinitis), linkages to multiple chromosomal locations genetic heterogeneity

Environmental triggers-

Allergens (House dust mite, pollen, pets (fur)), cigarette smoke, viral URTI, occupational allergens (isocyanates-spray paints, epoxy resins-adhesives/fibreglass fabrics)

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PathophysiologyAsthma

Type 1 hypersensitivity reaction in atopic asthma

Early phase (up to 1 hour)

After exposure to inhaled allergen in a presensitized individual results in cross linking of IgE antibodies on the surface of mast cells. Release of inflammatory mediators-bronchial smooth muscle contraction (bronchoconstriction), mucous hyper secretion and airway oedema and obstruction.

Late phase (after 6-12 hours)

Recruitment of

eosinophils

,

basophils,neutrophils

and Th2 lymphocytes results in the perpetuation of the airway inflammation and bronchial hyper-responsiveness.

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Aetiology/Risk factorsCOPD

Bronchial and alveolar damage due to environmental toxins-

smoking (cigarette smoke)

Indoor

air pollution (such as solid fuel used for cooking and heating

)

Outdoor

air

pollution

Occupational

dusts and chemicals (

vapours

, irritants, and fumes

)

Frequent

lower respiratory infections during

childhood.

Rare cause is

α

1-antitrypsin deficiency (<1%) consider in non smokers or in younger patients

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HistoryAsthma

Intermittent wheeze

Breathlessness (dyspnoea)

Cough (often nocturnal)

Occasionally sputum

Diurnal variation in symptoms/ peak flow- morning dips of peak flow recordings

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HistoryAsthma: Precipitating factors

Cold air

Exercise

Allergens (house dust mite, pollen, pets-animal fur)

Emotions

Smoking/passive smoking exposure

Viral URTI

Hx of

atopy

(eczema/

hayfever

-allergic rhinitis)

FHx

Drugs (Beta blockers, NSAIDS-

ask OTC meds

)- OSCE !

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HistoryAsthma: things to also ask!

Precipitating factors if present

C

ompliance with medication

R

eliever usage (inhaler) – gauge severity

O

ccupational Hx-cause

S

leep- interference? Severity

S

moking Hx

E

czema/

hayfever

-

atopy

D

ays off school/work – gauge severity

Remember

CROSSED

mnemonic!

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HistoryCOPD

Chronic breathlessness

Chronic Cough/sputum production

Wheeze

Smoker!

Minimal diurnal variation in symptoms compared to asthma

Age of onset >35 years (

Rare cause is

α

1-antitrypsin deficiency (<1%) consider in non smokers or in younger

patients)

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Clinical signs O/E

Asthma

COPD

TachypnoeaUse of accessory muscles of respirationHyper inflated chest (reduced chest expansion)Hyper resonant percussion noteReduced air entryPolyphonic wheeze

Tachypnoea

Use of accessory muscles of

respiration

Purse lip breathing

Hyper inflated chest (reduced chest expansion)

Hyper resonant percussion

note

Reduced air entry-prolonged expiration

Wheeze, crackles if infective exacerbation

cyanosis

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Severity of Asthma

Moderate exacerbation:

Increasing symptoms

PEF >50-75% of best or predicted

No features of severe asthma

Severe exacerbation:

Unable to complete sentences in one breath

PEF 33-50% of best or predicted

RR ≥ 25/min

HR ≥110/min

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Severity of Asthma

Life threatening attack: Any of

PEF <33% of best or predicted

Silent chest

Cyanosis

Feeble respiratory effort

Hypotension

Exhaustion/confusion/coma (CO2 retention)

ABG:

normal or high CO2 (normal PaCO2 4.6-6.0

k

P

a

)

PaO2 <8kPa/O2

sats

<92%

Low pH <7.35 acidosis (CO2 retention)

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Severity of COPD

Severity

FEV1 (% predicted)

Mild

≥80%

But FEV1/FVC <70%

Moderate

50-79%

Severe

30-49%

Very Severe

<30%

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InvestigationsAsthma

Acute exacerbation:

Peak flow- PEF reading to classify the severity

Basic Obs include pulse oximetry- classify severity

ABG-respiratory failure

CXR- exclude differentials i.e. pneumothorax, pneumonia

Bloods- FBC (raised WCC infective exacerbation),

U+E’s,

CRP

Blood culture (febrile)

Sputum culture

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InvestigationsAsthma

Chronic Asthma:

PEF monitoring with peak flow diary- diurnal variation >20% on ≥3days a week for 2 weeks with morning dips in readings.

Pulmonary function test- obstructive defect with improvement of FEV1 usually >15% improvement after a trial of a Beta 2 agonist.

Bloods- eosinophilia, raised IgE levels in atopic asthma.

Skin prick tests- help identify any allergens

Aspergillus antibody titres- for allergic aspergillus lung disease

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InvestigationsCOPD

Acute exacerbation:

ABG- respiratory failure

Bloods- FBC (raised WCC infection),U+Es, CRP

Bloods cultures if febrile

Sputum culture

CXR –exclude differential i.e. pneumothorax, pneumonia

ECG-

cor

pulmonale right axis deviation (RVH)

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InvestigationsCOPD

Chronic COPD:

Spirometry/pulmonary function tests- obstructive defect FEV1/FVC <70% also with FEV1<80% predicted

CXR- normal or show lung hyperinflation( >6 anterior ribs seen, flat hemi-diaphragms), large central pulmonary arteries, decreased peripheral vascular markings

ABG- hypoxia and/or hypercapnia

Bloods- FBC (increased

Hb

and PCV due to secondary polycythaemia secondary to hypoxia).

ECG and echocardiogram-

cor

pulmonale, pulmonary hypertension

α

1-antitrypsin levels- in young patients or with minimal smoking Hx

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Obstructive vs Restrictive defectSpirometry/PFT

FEV1

FVC

FEV1/FVC

Obstructive

lung disease

Decreased (<80%)

Decreased

Decreased

(<0.7)

Restrictive lung disease

Decreased

Decreased (<80%)

Normal

(>0.7) or increased

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ManagementAcute life threatening Asthma

Start Rx before Ix ABCDE!

O

xygen 15L NRB- sit patient up, 02

sats

94-98%/intubate

S

albutamol- 5mg Nebulised, back to back Nebs

H

ydrocortisone 100mg IV

I

pratropium bromide 0.5mg nebulised

T

heophylline (aminophylline) IV

Magnesium sulphate 2mg IV if no improvement

Remember

OSHIT

! Mnemonic

Normal or high CO2 is a very worrying sign- get early anaesthetic/ITU r/v

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Management Chronic AsthmaChronic Asthma

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Chronic Asthma Management

Asthma

Management The BTS Stepwise

Approach

Rx started at the step most appropriate to the

severity

STEP 1: SABA

STEP

2

: Step

1 + ICS

STEP

3: Step 2 + LABA &/or ↑ ICS dose

STEP

4

: Step

3 +

leukotriene receptor antagonist (

montelukast

)/theophylline

STEP

5: Step 4 + oral

steroids- refer to asthma clinic

Step down Rx if symptom control is good for >3 months

Educate on proper inhaler techniques and routine monitoring of peak flow.

Develop an individual

Mx

plan to avoid triggers

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Management Acute exacerbation COPD

ABCDE approach!

Controlled oxygen therapy 24-28%

Venturi

mask vary according to ABG- target

sats

88-92%

Nebulized bronchodilators- salbutamol 5mg (back to back NEBS) and

ipratopium

bromide 0.5mg (4-6 hourly)

Steroids- IV hydrocortisone 200mg or PO prednisolone 40mg (7-14 days)

Abx

- if evidence of infection see local guidelines

NIV- if severe respiratory acidosis or medical Rx shows no improvement e.g. BIPAP- type 2 respiratory failure

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Management Chronic COPD

Non Pharmacological

Mx

Smoking

Cessation

Nutrition- Rx poor nutrition e.g. fortisips

Obesity- healthy diet/lifestyle, regular exercise

Pulmonary Rehabilitation- graded exercise therapy to increased exercise tolerance

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Chronic Management COPD

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Chronic Management COPD

Mucolytics- aid chronic productive cough

CBT/Antidepressants- chronic illness

Criteria for LTOT:

Only for those stopped smoking-

fire risk!

PaO2<7.3

kPa

clinically stable- this value should be stable on two occasions >3 weeks apart

PaO2 7.3-8.0

kPa

with signs of pulmonary hypertension/

cor

pulmonale

Terminally ill patients

Surgical

Mx

- bullectomy (recurrent pneumothoraces), lung volume reduction surgery

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Inhalers-Quick run through

SABA-e.g. salbutamol (

ventolin

) “blue inhaler”

LABA-e.g.

salmeterol

(

serevent

)

SAMA- e.g.

ipratopium

bromide (

atrovent

)

LAMA-e.g.

tiotropium

bromide (

spiriva

)

IC Steroids:

Becotide

(

beclometasone

),

Pulmicort

(budesonide),

Flixotide

(fluticasone)

Combination ICS:

Seretide (

fluticastone

+

salmeterol

)

Symbicort

(budesonide +

formoterol

)

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Inhaler: Explaining how to use it

1. Remove the dust cap from the inhaler device.

2. Shake the device. Remember the canister holds a suspension of drug, and this needs to be shaken to ensure a uniform distribution of the drug particles.

3. If you have not used the inhaler for a week or more, or it is the first time you have used the inhaler, spray it into the air before using it to check that it works.

4. Hold the inhaler upright with you forefinger on the top of the canister.

5. Breathe out as far as is comfortable.

6. Place the mouthpiece in your mouth between your teeth, and close your lips around it.

7. Start to breathe in slowly and deeply, and at the same time, activate the inhaler by pressing down on the canister. When the canister is pushed down, a valve delivers a measured dose of drug in a fine mist.

8. Hold your breath for as long as is comfortable, then breathe out as normal.

9. If you are instructed to take 2 puffs, wait for about 30 seconds and repeat this process.

10. Do not release two puffs at the same time. This will increase the likelihood of deposition at the back of the throat and reduce the amount of drug reaching the lungs.

11. Finally, replace the cap on the inhaler.

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Clinical scenario

A 64 year old gentleman presents to A&E with increasing SOB over the last 3 days. This is associated with a cough productive of thick, green sputum. He has a past medical history of “asthma”, but he has smoked 50 cigarettes a day for the past 40 years. On examination he is

tachypnoeic

,

tachycardic

, O2

sats

85% on air, he is using his accessory muscles to breathe. Auscultation reveals bilateral diffuse coarse

crepitations

and widespread wheeze

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Questions

What are your main differential diagnoses for this

gentleman?

How would you investigate this gentleman?

Initial

management in acute setting?

Long-term management?

Can you tell me about the pathophysiology of COPD?

ie

. Clinical and

histopathological

definitions

Can you tell me some risk factors for COPD?

What are the criteria for mild, moderate, severe and very severe COPD?

What are the criteria for use of long term oxygen therapy (home oxygen)?

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THANK YOU FOR LISTENING

ANY QUESTIONS?