Respiratory Medicine: - PowerPoint Presentation

Slide1

Respiratory Medicine:Asthma and COPD

Dr Rickbir Singh Randhawa

FY1Slide2

Definition:AsthmaChronic 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 Slide3

Definition:COPDChronic 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.Slide4

AetiologyAsthmaGenetic 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)Slide5

PathophysiologyAsthmaType 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. Slide6

Aetiology/Risk factorsCOPDBronchial 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 patientsSlide7

HistoryAsthmaIntermittent wheezeBreathlessness (dyspnoea)

Cough (often nocturnal)

Occasionally sputum

Diurnal variation in symptoms/ peak flow- morning dips of peak flow recordingsSlide8

HistoryAsthma: Precipitating factorsCold airExercise

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 !Slide9

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!Slide10

HistoryCOPDChronic breathlessnessChronic 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)Slide11

Clinical signs O/EAsthmaCOPD

Tachypnoea

Use of accessory muscles of respiration

Hyper inflated chest (reduced chest expansion)

Hyper resonant percussion note

Reduced air entry

Polyphonic 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

cyanosisSlide12

Severity of AsthmaModerate 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/minSlide13

Severity of AsthmaLife threatening attack: Any ofPEF <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)Slide14

Severity of COPD

Severity

FEV1 (% predicted)

Mild

≥80%

But FEV1/FVC <70%

Moderate

50-79%

Severe

30-49%

Very Severe

<30%Slide15

InvestigationsAsthmaAcute 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 cultureSlide16

InvestigationsAsthmaChronic 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 diseaseSlide17

InvestigationsCOPDAcute 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)Slide18

InvestigationsCOPDChronic 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 HxSlide19

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 increasedSlide20

ManagementAcute life threatening AsthmaStart 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 Slide21

Management Chronic AsthmaChronic AsthmaSlide22

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 triggersSlide23

Management Acute exacerbation COPDABCDE 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 failureSlide24

Management Chronic COPDNon 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 toleranceSlide25

Chronic Management COPDSlide26

Chronic Management COPDMucolytics- aid chronic productive coughCBT/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 surgerySlide27

Inhalers-Quick run throughSABA-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

) Slide28

Inhaler: Explaining how to use it1. 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. Slide29

Clinical scenarioA 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 wheezeSlide30

QuestionsWhat 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)? Slide31

THANK YOU FOR LISTENINGANY QUESTIONS?