Asthma long answer Q

Question 1

What is Asthma

Answer 1

Chronic, but reversible airway obstructing condition

hypersensitivity in the trachea, bronchi & bronchioles in response to a range of stimuli

asthma presents with acute attacks, patient may be asymptomatic

2 main types:

• Extrinsic: type I hypersensitivity reaction to an extrinsic antigen or allergen
• Intrinsic - non-immune reaction, triggered by irritants

Question 2

Aetiology:

Answer 2

Caused by genetic and environmental factors:
oGenetic:
“ Genes &FHx - most
significant factor in <12 YO
oEnvironmental factors: Most significant in later onset
“ Hygiene hypothesis - less early pathogen exposure, increases risk of asthma development
“ Often initiated by an environmental trigger:
o Cigarrete smoke
o Pet hair
o Dust
o Pollen
o Polution
o Medication

Question 3

Pathophysiology

Answer 3

In intrinsic asthma:
o Irritants/emotion affect T-lymphocytes, chronically activating and causing a vagal reflex which may induce an inflammatory response
o Alternately Gastric reflux can cause bronchospasm, resulting in asthmatic symptoms

In extrinsic asthma:
o An allergen is inhaled
o Dendritic cells, found in epithelial tissue lining the respiratory tract phagocytose an allergen and present it on the cell surface
o Helper T cells detect the presented allergen and signal B cells to divide and form plasma cells
o The plasma cells produce IgE antibodies
o IgE attach to mast cells, forming mast cell-IgE complexes
o Allergens attach to the IgE antibodies on the mast cell surface, activating the complement system
o This results in degranulation of the mast cell, releasing:
- Histamine - causes activation of autonomic NS, causing contraction of smooth muscle surrounding bronchioles and bronchi - bronchoconstriction, reducing the amount of air reaching the alveoli
- Prostoglandins - cause vascular permeability of alveolar capillaries, leading to bronchiole oedema, further restricting airflow
- IL-5 - stimulates Eosinophils, which damage the lung tissue
- Consistent allergen exposure and therefore damage causes allergen remodelling and fibrosis - essentially scarring of lung tissue, permanently limiting lung expansion and airflow, making subsequent attacks more likely to be life threatening

• Goblet cells in the pulmonary epithelium are stimulated by eosinophils, increasing mucus production
  o Mucus forms plugs in the alveoli, blocking air from reaching the alveoli and oxygen entering the bloodstream. It also causes air trapping, preventing lungs from deflating and CO2 escaping
  o Forced expiration in an attempt to shift the built up CO2 causes the bronchial wall to collapse, resulting in inspiration and coughing becoming more difficult
  o The combination of Mucus, Bronchoconstriction and Bronchioedema results in a severely limited airflow to the alveoli, reducing gas exchange and causing hypoxia and hypercapnia
  o In an attempt to compensate, the patients respiratory rate increases
  o Hypercapnia causes the increase of carbonic acid in the blood, resulting in respiratory acidosis.
  o The high resp rate will cause distress and activate the SNS, causing adrenaline release
  o Adrenaline causes peripheral vasoconstriction, resulting in cyanosed peripheries and blood being redirected to the vital organs
  o However, if hypoxia becomes severe enough, vital organs will become ischaemic and will ultimately result in cardiac arrest.

Question 4

Signs and Symptoms

Answer 4

” Coughing
“ Chest tightness
“ Dyspnoea
“ Wheezing - from air passing through narrowed bronchiole
“ Laboured, rapid breathing
“ Thick mucus production
“ Tachycardia & pulsus paradoxus - different pulse on inspiration and expiration
“ Cyanosis
“ Fatigue
“ “Shark fin” ETCO2 waves
“ Respiratiory alkalosis initially due to hyperventilation
“ Then acidosis due to lactic acid buildup from hypoxia
“ Respiratory failure - Higher than normal ETCO2

In life threatening asthma:
“ Severe wheeze or silent chest on auscultation
“ Peak flow of <33% of predicted best or unable to perform peak flow
“ Bradycardia due to hypoxia-caused myocardial ischaemia
“ Cyanosis
“ Confusion, agitation and restlessness leading to unconsciousness -cerebral hypoxia
“ Exhaustion
“ Arrythmias - ischaemic cardiac tissue
“ Hypotension due to reduced HR
“ Poor respiratory effort
“ SpO2 < 92%
“ hypotension

Question 5

Management

Answer 5

If time critical features present:
      "	Major ABCD issue
      "	Assisted ventilation 
        required 10>resps<30 
      "	Exhaustion
      "	Cyanosis
      "	Silent chest
      "	Sats <92%
      "	PEF <33% or unable to 
      perform
Transfer immediately to nearest A&amp;E on blue lights - provide pre-alert

Correct symptoms on route:
“ Pharmacological:
“ Salbutamol:
o 5mg/2.5 ml nebulised continuously with 6-8L/min O2 (I’d go for 8 as pt is likely to be very hypoxic)
o Unless severe side effects occur (e.g. allergy or SVT)
o Beta-2 adrenergic agonist

  "	Adrenaline:
 o	1 in 1000, 500mcg/0.5ml IM
     Bronchodilates
 o	Repeat every 5 min until improved - no max repeats	

Can consider other medications used in asthma such as ipratropium and hydrocortisone, however it is important that transport is not delayed in order to administer them, therefore they should only be administered en route in life threatening asthma

” Non-pharmacological
“ Reassure pt - will be very distressing for them
“ Sit pt up
“ Measure ETCO2 en route:
“ Shark fin waves indicate bronchospasm
“ Very High CO2 suggests approaching arrest
“ Monitor ECG - either 4 leads or pads
“ Subtly get out pads and bvm - good chance of pt arresting