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CRV week 3 > Asthma > Flashcards

Asthma Flashcards

1
Q

what is the pathophysiology of asthma?

A

inflammatory disease of the medium sized airway
associated with
-loss of airway epithelium
-thickening of BM
-hypertrophy of the smooth muscle layer
resulting in;
-hyper responsiveness to normal triggers of contraction
-abnormal contraction in response to usually benign triggers

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2
Q

what happens to the smooth muscle in athsma?

A

hypertrophy (increase in the size of cells): increase in the amount of smooth muscle which forms a lattice work underneath the epithelial layer

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3
Q

what can athsma result in?

A
  • Hyper-responsiveness to normal triggers of contraction (eg ACh or Histamine)
  • Abnormal contraction in response to usually benign triggers (triggers which normally would cause a resposne)
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4
Q

what are some of the inflammatory triggers for athsma?

A

allergy
viral/bacterial infection
exercise

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5
Q

what are some of the drug triggers for athsma?

A
  • Beta-blockers (for Hypertension or Anxiety)
  • Non-steroidal anti-inflammatory drugs (which interfere with normal control of inflammation)
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6
Q
A
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7
Q

what is the management of asthma symptoms?

A
  • Bronchorelaxation – beta2 Agonists - Salbutamol relaxes smooth muscle tightening
  • Anti-inflammatories – corticosteroids, leukotriene receptor blockade, monoclonal antibodies - cuts down inflammation and cuts down inflammation related symptoms
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8
Q

what are the consequences of the lungs only having one orifice?

A

Since same orrifice, we maximise inspiration is at the expense of expriation

  • Lower curve is inspiration and upper is expiration
  • Inspiration - a plateu is formed fairly quicky
  • Expiration - fast increase then as airways are compressed, flow rate dec slowly until lungs are emptied
    maximise time spent during inspiration, at the expense of expiration - resulted in rapid flow rates
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9
Q

what has the single orrifice done for our flow rates?

A
  • this single orrifce has allowed us to generate very large flow rates of 900 litres/min
  • Achieved by firm but flexible airway walls
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10
Q

what would happen if we had no firm and flexible airways?

A

if here was no tension/tightness, expiration would compress the airway walls

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11
Q

what happens to the airways in athsma?

A
  • Dynamic: (come and go)
    • Rapid muscle contraction (Ach by vagus, and Histamine)
    • Medium timescale – secretions
  • Fixed: Stiff airway wall
    • Smooth muscle bulk
    • Thickened basement membrane
    • therefore reduced ccompliance aand failure of relaxation
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12
Q

what is asthma pathology?

A
  • Weakened and ‘denuded’ airway epithelium - due to inflammation causing it to die
  • Thickened BM - pink - more collagen which is tensile, non elastic and doesnt easily relax
  • Increased Smooth Muscle -pink and red- trying to work hard against narrow lumen
  • Mast cells within Smooth Muscle meshwork- Histamine released which causes smooth muscle contractions
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13
Q

describe asthma physiology?

A
  • Increased smooth muscle - Increased force contraction (by histamine and Mch like Ach)
  • Mast cells in smooth muscle (in airways now due to inflammotry infitration) - Twitchy smooth muscle variable airway calibre (changing sensitivity and activity and changes in width of airways)
  • Increased basement membrane - Loss of relaxation after contraction (poor elasticity due to more collagen. Chronic reduction in airway callibre leads to chronic damge to airways and long term breathlessness)
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14
Q

what are the symptoms of asthma?

A
  • Triggered breathlessness/wheeze
    • Eg – histamine (allergy)or cold
  • Diurnal variation – nightime or early morning
  • Cough
  • Variable airway calibre
    • Bronchial Hyper-reactivity
      • Exaggerated response to usually constricting stimuli eg metacholine or histamine
  • Inflammatory secretions
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15
Q

what are bronchial airway hyperactivity tests?

A
  • much faster drop/reaction in asthmatic individuals compared to normal when exposed to histamine or mannitol.
  • In asthmatic individuals - A drop of ≥ 20% FEV1 by ≤ 8mg/ml metacholine (may also use histamine or mannitol)
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16
Q

what can variable airway calibre cause?

A
  • More smooth muscle so therefore more peak flow variability - by peak flow diary
  • usually in normaly people, morning peak flow is lower than evening

Diurnal Variability – lower in morning than midday

Day to Day variability

17
Q

what are the differences in peak flow variability between asthmatic and normal people?

A

overall decline in lung funtion over the week (as this student had a cat)

18
Q

what type of inflammation happens during asthma?

A
  • type of inflammation is usually Eosinophillic - granulocyte usually present in allergic responses, parasites foreign bodies
  • These eosinophils make Nitric Oxide increase
  • The exhaled NO can be measured and normal Value 30 ppb (parts per billion!)
19
Q

what is the difference between asthma and COPD?

A

Reversible airflow contraction in asthma with salbutamol

20
Q

why is athsma a 3 phase disease?

A
  • (need all 3 and one alone is suffient for asthma)
  • Smooth muscle only – triggered by direct mediator release eg histamine – rare wheezy episodes
  • Chronic Inflammation – irritates the smooth muscle and causes regular wheezy episodes
  • Acute Inflammation – viral infection – ‘clinical exacerbations’
21
Q

why is inflammation a good thing?

A
  • Inflammation leads to tissue repair and return of normal organ function
  • Network of cells and chemical signals (cytokines, prostaglandins, leukotrienes, immunoglobulins) carefully regulated (with on and off cytokines)
  • In an abnormal organ (eg asthmatic airways) or in the wrong place inflammation can cause harm
22
Q

Which inflammation type is associated with Asthma- and what does it contain?

A
  • Type 2 inflammation – commonly associated with asthma and allergy
  • Cells – lymphocytes, eosinophils and mast cells, TH2
  • Cytokines – IL-4, IL-5, GMCSF
  • Prostanoids – PGELeukotriene D4
  • Immunoglobulins – specific IgE (eg House dust mite - drives type 1)
23
Q

how does immunity drive inflammation?

A
  • Immunity is a reaction to an external factor
  • Inflammation is a reaction to trauma like a cut
    APC = antigen presenting cell

nature of response is dependant on the cytokine environment

24
Q

what happens with inflammation in asthma?

A
  • the Mast cells as we know are now in the lungs smooth muscle
    • these mast cells have memory IgE receptors on them
  • During the secondary response, the APC recognises the allergy, and stimulates an IL-4 IL-33 response which generates IgE.
  • IgE is avidly bound to receptors on the surface of mast cells
  • memory is retained within the IgE, which is used by B lymphocytes
  • IgE is retained long term on the surface of mast cells, and on B lymphocytes
25
Q

what is the inflammation cascade involved in asthma?

A
  1. Antigen binding to allergen
  2. binding to IgE on mast cells
  3. cross-linking the receptors for IgE
  4. bringing two receptors close together
  5. Activates a cascade of cell signalling pathways.
  6. Results in mast cell mediator release
26
Q

what are some examples of mast cell mediators?

A

histamine
leukotriene
prostaglandin
VGEF

27
Q

what effects does mast cell mediators have on the airway?

A

smooth muscle contraction
airway wall oedema
inflammation and secretions
blood vessel formation

28
Q

mast cells embedded in the smooth muscle causes what?

A
  • They cause immediate smooth muscle contraction - Bronchospasm and wheeze (quick)
  • Alveolar wall oedema - Airway narrowing (gradual)
  • Blood vessel hypertrophy - Airway wall thickening and lumen narrowing (long term)
29
Q

what are some chemical ways of triggering mast cells?

A

IgE - allergen exposure
salicylates - aspirin
scents - curry

30
Q

what are some osmotic ways of triggering mast cells?

A

exercise that increases ventilation litres/min
exceeds humidifying capacity of upper airway (eg nose)
drying air cause osmotic rupture of mast cell
mimicked by mannitol in bronchial challenge testing x

31
Q

what are some inflammatory triggers of mast cells?

A

viral infection
parasitic infection
bacterial
neutrophils/lymphocytes
eosinophils
neutrophilic

32
Q

what are the 3 hits of asthma?

A

-acute inflammation acts on chronically inflamed airway to cause smooth muscle spasm
-inflammation causes cough
-muscle spasm causes breathless, wheeze and exercise intolerance

33
Q

how do beta 2 agonists treat asthma?

A

activates G protein
cyclic AMP - second messenger
relaxes smooth muscle widening the airway

34
Q

what are the conventional treatments for asthma and for inflammation?

A

corticosteroids
anti-leyukotrine receptor drugs

35
Q

what are corticosteroids?

A

mainstay of treatment prevents and treats inflammation non selectively. Reduces airway twitchiness and reduces exhaled nitric oxide

36
Q

what are anti-leukotriene receptor drugs?

A

add on treatment for resistant inflammation.
targets only leukotriene D4 in the airway. direct effect on mast cells and smooth muscle. good in exercise asthma

37
Q

what are some emerging inflammatory treatments of asthma?

A
  • Anti IgE - blocks IgE peripherally, reducing IgE on mast cells, reducing twitching and reducing exacerbation (frequency?)of asthma
  • Green box - development of drugs which aim to block TNF, Il5 and IL13
  • IL5 and IL13 are cytokines which are important in the airways of asthmatics and have an impact on eosinophils and directly on smooth muscle cells
38
Q

how do we treat pathology with the bronchoscope?

A
  • Heating amlall airways to reduce bulk of smooth muscle, reducing twitching and exacerbations
  • bronchothermoplasty = sending a probe in to the lung which super heats the airway in the smaller airways. This has a consequence of reducing the bulk of airway smooth muscle. Results in reduction of twitching
  • Vagus nerve ablation: can be done through bronchoscopy test.

CRV week 3 (8 decks)

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