IBSc: Question 6 - Asthma By Alan McLeod. Getting the best marks Read the whole question – a...
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Transcript of IBSc: Question 6 - Asthma By Alan McLeod. Getting the best marks Read the whole question – a...
iBSc: Question 6 - Asthma
By Alan McLeod
Getting the best marks
Read the whole question – a latter section may give you a
clue about an earlier one.
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 giving a list answer put the best answers first – examiners will not usually mark answers too
far down a list
Always write something – it may get you part of a mark and is anonymised so
no one will think you are stupid!
If you genuinely have no clue then re-write the question to see if this sparks
some ideas.
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 Infectious / inflammatory
D Degenerative
G Genetic / Idiopathic
E Endocrine
T Trauma
V Vascular
I Iatrogenic / ingested
N Neoplastic
O Organs
Acute Dyspnoea
I Infectious / inflammatoryAsthma, Pneumonia, COPD exacerbation (e.g. upper resp tract infection)
D Degenerative
G Genetic / ideopathic
E Endocrine
T Trauma Pneumothorax
V Vascular Myocardial infarction, PE
I Iatrogenic / ingested Foreign body (mostly children)
N Neoplastic
O Organs / other Lungs
Emergency ManagementD Danger? Check that the scene is safe
R Run Check for response
H Happily Call for HELP!
A Away andCheck and secure airway and C-spine
B Buy Check breathing, Resp rate
C Chocolate! Pulse, Heart rate
Emergency Management
D ‘Disability’Neuro exam: minimum is pupil size / response + GCS or AVPU
E ‘Exposure’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 Last meal (time)
E 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=related
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 IP31
• Some proponents argue for a cAMP independent PKA mechanism as well2
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
Ca++ In
Beta-adrenergic antagonists
‘Beta blockers’• Combat the harmful
activation of the sympathetic nervous system
• Decrease HR• Decrease contractility
Examples• Propranalol• Sotalol
Side effects• Bronchoconstriction• Bradycardia
Asthma
Airway
COS of Three Pathologies
Constriction Oedema Secretions
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 r4
• Inversely proportional to viscosity
The Alveolus
Vessels in the Lung
• Pulmonary Artery– Deoxygenated blood– From Right Ventricle– Oxygenated in lungs– Affected in PE
• Bronchial Artery– Oxygenated blood– From systemic supply– Supplies tissues of lung
• Pulmonary vein– Oxygenated blood– From lungs– To Left atrium
Stages of Change Model
• AKA ‘Transtheoretical’
• By Prochasta and Diclemente
• Patient focus• Explains why some
interventions don’t work
• Allows you to predict which ones might!
Contempla-tion
Mainten-ance
Pre Contemplation
Preparation Action
Two Useful Concepts
Body Mass Index (BMI)
20-25: Ideal
26-30: Overweight
31-35: Obese
Pack Years
> 20 = increased chance complications
PY=Cigs / day
x Yrs20
BMI=Wt (kg)
Ht2 (M)
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.