iBSc: Question 6 - Asthma

By Alan McLeod

Getting the best marks

Read the whole question an earlier one.

– a latter section may give you a clue about Always write

something

– it may get you part of a mark and is anonymised so no one will think you are stupid!

To see how many points you need look at the marks allocated – for example a 3 point question is generally looking for 3 salient points If you genuinely have no clue then re-write the question to see if this sparks some ideas.

If giving a list answer put the best answers first – examiners will not usually mark answers too far down a list If not then

move on

and come back at the end. And remember – always write

something

.

Good luck!

Question 6

Mrs Rockley, a 67 year old smoker presents with an acute attack of breathlessness. Q6.1

• List 3 differentials (3) Q6.2

• Describe IMMEDIATE management on arrival at A+E (3)

Question 6

She has a polyphonic wheeze and a history of asthma. Q6.3

• As part of your treatment you give salbutamol – this is a beta agonist. How on a molecular level do these drugs work? (6)

Question 4

The airway narrowing in asthma is multifactorial Q6.4

• List the three main factors (3) Q6.5

• If the radius is halved with other factors remaining equal what happens to the

flow

of air? (3)

Question 6

Most gas exchange takes place within the alveoli Q6.6

• Draw and lable an alveolus showing cells and fluids present and nearby important structures (7)

Question 6

Mrs Rockley smokes 30 cigarettes a day – you try to persuade her to stop.

Q6.7

• Describe the Stages of Change model and how it may help you with getting Mrs Rockley to stop smokeing (8)

The Answers

View these on ‘note view’ rather than on full screen – additional notes are provided for some slides

Generating Differentials: I’D GET VINO… I D G E T V I N O Infectious / inflammatory Degenerative Genetic / Idiopathic Endocrine Trauma Vascular Iatrogenic / ingested Neoplastic Organs

Acute Dyspnoea

I Infectious / inflammatory Asthma, Pneumonia, COPD exacerbation (e.g. upper resp tract infection) D Degenerative G Genetic / ideopathic E T Endocrine Trauma V I Vascular Iatrogenic / ingested N Neoplastic O Organs / other Pneumothorax Myocardial infarction, PE Foreign body (mostly children) Lungs

Emergency Management

D Danger?

Check that the scene is safe R H A Run Happily Away and B Buy Check for response Call for HELP!

Check and secure airway and C spine Check breathing, Resp rate C Chocolate! Pulse, Heart rate

Emergency Management

D ‘Disability’ E ‘Exposure’ Neuro exam: minimum is pupil size / response + GCS or AVPU 1: Expose to seek injuries 2: Keep warm + take temperature DEFG Don’t Ever Forget Glucose!!!

An AMPLE history A Allergies M Medications P Past med Hx L E Last meal (time) Event – what happened

GPCRs

Salbutamol is a beta agonist – it binds to beta receptors – the are G-protein coupled receptors http://uk.youtube.com/watch?v=tOcGbnBCdMM http://uk.youtube.com/watch?v=bU4955rLv_8&feature=rela ted

GPCR Summary

• Receptor complex + G protein • G Protein has 3 subunits (alpha, beta & gamma) • Receptor binds ligand • Conformational change • Loss of GDP from G protein alpha subunit • Binding of GTP • Separation of alpha subunit from beta gamma dimer • Alpha and beta-gamma freed to interact with effectors.

• Cascade effect.

• Cycle starts again

GPCRs in the lung

Beta receptors • GPCRs • Gs actvates adenylate cyclase – Increased cAMP – ATP  cAMP • cAMP causes relaxation of the smooth muscle • Decreases sensitivity of the IP3 receptor, decreasing release of calcium from intracellular stores in response to IP3 1 • Some proponents argue for a cAMP independent PKA mechanism as well 2

GPCRs in the heart

Beta receptors • GPCRs • Gs activates adenylate cyclase – Increased cAMP – ATP  cAMP • cAMP activates PKA • PKA phosphorylates alpha-1 subunit on voltage-gated Ca ++ channels • Increased Ca ++ influx • Increased inotropy • Increased rate Ca ++ In

Beta-adrenergic antagonists

‘Beta blockers’ • Combat the harmful activation of the sympathetic nervous system Examples • Propranalol • Sotalol • Decrease HR • Decrease contractility Side effects • Bronchoconstriction • Bradycardia

Airway

Asthma

COS

of Three Pathologies

C

onstriction

O

edema

S

ecretions

Velocity and Flow

Velocity • Displacement of

single

particle per unit time • Inversely proportional to cross sectional area – Faster in thinner tubes • Aorta is thinner than total mass of capillaries – V slow capillary flow – Time for gaseous exch Flow • Volume of fluid passing point A at time B • • Proportional to pressure

difference

• Inversely proportional to tube length

Proportional to r 4

• Inversely proportional to viscosity

The Alveolus

Vessels in the Lung

• Pulmonary Artery – Deoxygenated blood – From Right Ventricle – Oxygenated in lungs –

Affected in PE

• Pulmonary vein – Oxygenated blood – From lungs – To Left atrium • Bronchial Artery – Oxygenated blood – From systemic supply – Supplies tissues of lung

Stages of Change Model

Preparation Action Contempla tion Mainten ance Pre Contemplation • AKA ‘Transtheoretical’ • By Prochasta and Diclemente • Patient focus • Explains why some interventions don’t work • Allows you to predict which ones might!

Two Useful Concepts

Body Mass Index (BMI)

BMI= Wt (kg) Ht 2 (M)

Pack Years

PY= Cigs / day 20 x Yrs > 20 = increased chance complications 20-25: Ideal 26-30: Overweight 31-35: Obese

The End

The slides here should allow you to mark your own work – remember 1 mark per answer up to the maximum for the question. Multiply by 3 to get percentage points. I assume a 60% pass mark. Sorry but I am unable to give further advice on answers due to time constraints.