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respiratory > Asthma basics of therapeutics and pharmacological treatments > Flashcards

Asthma basics of therapeutics and pharmacological treatments Flashcards

1
Q

Epidemiology

A

study of distribution and determinants of health related states and events in specified populations

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2
Q

Extrinsic asthma

A

allergic - more in children ( 1/11 affected in Uk)

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3
Q

intrinsic asthma

A

non-allergic - no detectable

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4
Q

how many people have asthma in the uk

A

5.4million

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5
Q

Episodic

A

seasonal

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6
Q 
Pets 
Stress
Exercise
Pollen 
Pollution
Smoke
Dust
Cold air 
Fungus spores
Bug
Chemical fumes
A

all triggers of asthma

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7
Q

what antibody mediates asthma

A

IgE - formed in response to allergen
frist exposure drives sensitization and memory
preexposure - allergen binds to specific IgE molecule on the mast cell surface

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8
Q

what ion moving into the mast cell drives degranulation ?

what does the mast cell release

A

calcium

histamines and prostoglandins

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9
Q

Mechanism of airway narrowing in asthma

takes around 20mins to hours

A

Airway narrowing
Open airway - smooth muscle layer goes into spasm , narrowing the airway ,
lining of the lung becomes inflamed and then mucus production is increased blocking the airway even more than usual - in some part of the airway mucus can from plush that nearly or completely block the airway
Imagine airway picture as a circle

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10
Q

In the early phase of an asthma attack what happens

A

Allergen or non specific stimulus binds to the mast cell releasing spasmogens leading to bronchospasm.
Chemotaxins and chemokines are released by the mast cells

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11
Q

this leads into the late phase - what happens here

A

Infiltration of Th2 cells -activation of inflammatory cells such as eosinophils
These release cysLTs and other mediators
This leads to airway inflammation and airway hyperreactivity leading to bronchospasm and wheezing

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12
Q

What to eosinophils release that contribute to airway hyperactivity and damage epithelial lining

A

EMBP

ECP

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13
Q

common signs and symptoms of asthma

A

Coughing - worse at night or first in morning
Wheezing or whistling noise in the chest heard on expiration - tight airway pressure to exhale
SOB
Tightness in the chest ( dyspnoea)

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14
Q

dyspnoea

A

shortness of breath

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15
Q

In asthma how does FVC and FEV1 and the ratio change - on spirometry

A

FVC dose not change
FEV1 reduces
So ratio falls and PEFR drops

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16
Q

comparing moderate , acute/severe and life threatening asthma change

PEF 
SpO2
speech 
Respiration 
Pulse
A

PEF >50-70% , 33-50 , under 33
SpO2 >92 , “ , below 92
speech normal, can’t complete sentences , silent chest cyanosis or poor respiratory effort
Respiration <25/m , over 25 then hypotenison and arrhythmia
Pulse <110 then above then altered consciouness

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17
Q

in self management of asthma what can you do

A 
Avoidance of triggers 
Desensitisation to specific allergen 
House dust mite control measures 
Smoking cessation 
Weight reduction
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18
Q

what are the 3 relievers

A

Relievers Beta 2 agonists
antimuscarinics
methylxanthines

19
Q

what are the preventers

A

corticosteroids
leukotriene receptor antagonists
cromones
long acting beta agonists

20
Q

examples of Short acting beta 2 agonists
and how does it work

via what second messenger

A

Salbutamol, terbutaline

Stimulation of B2 receptor on airway smooth muscle - cAMP

21
Q

adverse effects of short acting beta 2 agonists

A

fine tremors of the hands , nervous tension , headaches and tachycardia
Hypokalemia at high doses

22
Q

how do Methylxanthines eg theophylline work

how are they given

A

Inhibits phosphodiesterase - break down cAMP

Given orally ( usually s/r) or by very slow i/v infusion 
Hepatically metabolised ( CYP1A2- half lives of drugs)
23
Q

what type of receptor is a Beta 2 adrenoreceptor

how does it work

A

G alpha s receptor
Beta 2 Galpha S coupled - adenyl cyclase coverts ATP to cAMP

cAMP inhibit MLCK so stops interaction and leads to broncho dilation and relaxation of the smooth muscle

24
Q

aminophylline otherwise known as PDE - breaks down what

A

PDE

25
Q

what dos a narrow therapeutic range mean

A

therapeutic window of a certain drug reflects the conc range that provides efficacy without unacceptable toxicity

26
Q

Antimuscarinics eg ipratropium

work how

A

Main target is M3 subtype- block it - onset is slower than that of beta 2 agonists
inhaled

27
Q

atropine I a antimuscarinics - why is it not used

A

not used in an airway disorder as increase mucus viscosity and reduces clearance

28
Q

when should you be careful when using antimuscarinics

A

prostatic hyperplasia, bladder outflow obstruction , angle closure glaucoma

29
Q

examples of corticosteroids

A

beclomethasone
fluticasone
budesonide

30
Q

side effects of corticosteroids

transcription of proteins

A 
Hoarse voice ( dysphonia) , reflex cough following inhalation 
Oral candidiasis
31
Q

what do you give as an IV injection in emergency treatment of a severe acute asthma attack

A

Hydrocortisone

32
Q

Leukotriene - receptor antagonists eg montelukast and zafirlukast

effective in late phase asthmas response - inhaled with corticosteroid

how does it work

A

Block effects of cysteinyl leukotriene in airways - anti-inflammatory reaction

33
Q

cromones is a prophylactic drug

would it have value in an acute asthma attack

A

no

34
Q

What are limitations of croons

A

Must be withdrawn gradually over 1 week - side effects - throat irritation and untolerable for some patients , sudden withdrawal rebound sensitivity

35
Q

Long acting Beta 2 agonists salmeterol and formoterol

used when

A

long term control of chronic asthma

36
Q

How to monoclonal antibodies work

A

selectively bind to IgE forming a complex ( mast cell not activated reducing mediated response)

over 12

37
Q

what does well controlled asthma look like

A

Well controlled asthma look like
No daytime symptoms
No night time awakening due to atham
No need for rescue medication ( reliever ones)
No limitation on activity including exercise
Normal lung function with minimal side effects
FEV1 and/or PEF >80% predicted or best

38
Q

ICS

A

inhaled corticosteroids

39
Q

. A patient comes into hospital after falling through thin ice on a frozen lake. He is hypothermic.
i). Which direction will the oxygen dissociation curve shift in response to this patient’s change in temperature?
Ii). Does this environment favour the loading or unloading of oxygen?

A

i). Left, (½ mark).
Ii). Loading, (½ mark).
Reduced temperature is a factor which shifts the oxygen dissociation curve to the left, favouring the binding or loading of oxygen to haemoglobin. This naturally occurs in the alveoli which have a reduced temperature compared to other parts of the body, encouraging the loading of oxygen to red blood cells in the lungs in order to be delivered to the rest of the body. In hypothermia, the entire body temperature is reduced, this means oxygen isn’t unloaded as readily in it’s target locations around the body.

other factors that shift it left are

Any two of: Alkalosis/Increased blood pH/less acid; Decreased CO2/metabolites; Decreased 2, 3 DPG; CO poisoning; foetal haemoglobin. (½ mark each). This environment is found naturally in alveolar cells to encourage loading of oxygen. However it can also occur during pathological processes in areas of the body where the unloading of oxygen is needed such as CO poisoning.

40
Q

Sx of asthma

A

a whistling sound when breathing (wheezing). Breathlessness. a tight chest, which may feel like a band is tightening around it.Coughing, hyperresonant chest on percussion

The cold produces histamine , fluid evaporates faster than it can be replaced so dry airways - produce histamine - allergic

41
Q

what is occurring immunological with asthma

A

Allergen inhaled to bronchioles, consumed by dendritic cells activating them they release chemokines - TH2 cells bought in or recognised by columnar epithelium released by TSLP increases mre chemokine
TH2 activate plasma cells to release IgE using Il-13,4
Mast cell but Il-9
Eosinophil production and bone marrow
Ige binds on to mast cell to bind to complex and release prostaglandins causing bronchoconstriction , all inflammation creates mucus build up
Endothelial - main mast cells to area - release stem cell factors

42
Q

Long term asthma control medication that is taken regularly to control chronic symptoms and prevent asthma attacks — the most important type of treatment for most people with asthma

A 
Inhaled corticosteroids
Leukotriene modifiers
Long-acting beta agonists (LABAs)
Theophylline
Combination inhalers that contain both a corticosteroid and a LABA
43
Q

quick relief medications ( rescue medications) -Taken as needed for rapid, short-term relief of symptoms — used to prevent or treat an asthma attack

A

Short-acting beta agonists such as albuterol
Ipratropium (Atrovent)
Oral and intravenous corticosteroids (for serious asthma attacks)

44
Q

Medications for allergy-induced asthma- Taken regularly or as needed to reduce your body’s sensitivity to a particular allergy-causing substance (allergen)

A 
Allergy shots (immunotherapy)
Allergy medications

respiratory (22 decks)

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