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Condensed Pathophysiology of Ill-health > Respiratory Asthma > Flashcards

Respiratory Asthma Flashcards

1
Q

Definition of Asthma

A

“a chronic inflammatory disorder of the airways…in
susceptible individuals, inflammatory symptoms are
usually associated with widespread but variable airflow
obstruction and an increase in airway response to a
variety of stimuli. Obstruction is often reversible, either
spontaneously or with treatment”
(International Consensus Report 1992 in BTS guidelines for asthma 2007)

However, we need to appreciate that there is no universal
accepted definition of asthma

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2
Q

Asthma - heritable disease?

A

A complex heritable disease with a number of genes which contribute, including Chromosome 5, 6, 11, 12 & 14

In particular chromosome 5 - encodes for key molecules in the inflammatory response including cytokines, growth factors and growth receptors

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3
Q

Asthma - environmental disease?

What provokes asthma?

A

Combo of genes x environment

Indoor allergens e.g. dust mites, pollution and dander
Outdoor allergens such as pollens and mould
tobacco smoke
chemical irritants
 Other triggers can include cold air, extreme
emotional arousal such as anger or fear, and
physical exercise

 Certain medications can trigger asthma: aspirin
and other non-steroid anti-inflammatory drugs,
and beta-blockers (which are used to treat high
blood pressure, heart conditions and migraine)

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4
Q

What types of medications can trigger asthma and why?

A

Certain medications can trigger asthma: aspirin
and other non-steroid anti-inflammatory drugs,
and beta-blockers (which are used to treat high
blood pressure, heart conditions and migraine)

Aspirin: Deregulates leukotrienes, substances which cause inflammation and symptoms of asthma

Beta-blockers receptors found in:

B1 - heart and kidneys
B2 - liver, lungs, skeletal muscles, uterus, GI tract & vascular smooth muscle
B3 - fat cells of body

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5
Q

How much do we breathe out?

Oxygen
Carbon Dioxide
Nitrogen

A

Oxygen (O2) 20.98%
Carbon Dioxide (CO2) 0.04%
Nitrogen (N) 76%

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6
Q

Normal vital signs?

 Respiratory rate, depth and pattern
 Blood pressure, systolic and diastolic
 Heart rate, rhythm and amplitude
 Temperature

A

 A PATENT AIRWAY
 Respiratory rate, depth and pattern-12-20 breaths
per minute, normal depth, regular.
 Pulse rate, rhythm and amplitude-60-100 beats per
minute, regular, normal amplitude.
 Blood pressure systolic blood pressure-140-110
mmHg, diastolic 90-60mmHg
 Temperature- 36.0° – 37.5° Celsius

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7
Q

Normal Arterial blood gas values?

(kpa/mmHg)

pH:
PaO2:
PaCO2:
Lactate:

A

 pH 7.35-7.45
 Lactate (0.5-1.00
mmol/L)

 Kpa
 PaO2 11-14 Kpa
 PaCO2 4.7-6.0 Kpa

 mmHg
 Pa02 80-100 mmHg
 PaCO2 35-45 mmHg

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8
Q

Respiratory Failure

Type 1

Type 2

A

Type I
• It is generally accepted that Type I respiratory failure is characterised as either the arterial O2 level being below 8Kpa and the CO2 being less than 6Kpa (normal).

Type II
• It is generally accepted that patients with Type II respiratory failure also have an arterial oxygen concentration below
8Kpa however the arterial carbon dioxide level is greater than 6kpa.

• The hypercapnia (raised CO2) and hypoxaemia occur as a result of decreased alveolar ventilation

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9
Q

Aerobic Respiration

Stages?
How many ATP produced?

A

Glucose ->

Glycolysis in cytoplasm (+4 ATP (2 net))->

Pyruvate->

Kreb’s cycle(+ 2 ATP)->

Electron Transport Phosphorylation (+32)

= 36 ATP

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10
Q

The circulatory system carries Carbon Dioxide to the lungs in 3 ways:

How?
& %

A
  • 7% as gas dissolved in plasma
  • 23% combined with globin to form Carbinohaemoglobin
  • 70% combined with water as Carbonic acid
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11
Q

How is Carbonic Acid broken down?

A

In the presence of the enzyme Carbonic Anhydrase, Carbonic acid breaks down to Hydrogen and Bicarbonate ions

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12
Q

Normal CO2 transport in the body?

A

H20+C02 = H2CO3 (carbonic acid)

This diassociates to:

H + HCO3 (bicarbonate)

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13
Q

Carbon dioxide essentially functions as an ____ in the body?

A

Acid

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14
Q

When we measure pH we are measuring the number of ____ ions …?

A

Hydrogen (the H in pH)

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15
Q

Normal plasma pH?

What is lower/ higher pH

What no. = cell death?

A

7.35-7.45

Lower= acid
Higher = alkali

6.8 = cell death

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16
Q

What factors affect the pH?

A
  • Carbon dioxide
  • The renal system
  • The buffer system
  • Cell activity
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17
Q

What happens to your respiratory rate when you become ACIDOTIC?

A
  • Falling pH (due to rising hydrogen levels)
  • Chemo-receptors
  • Medulla Oblongata
  • Phrenic and respiratory nerves
  • Increased respiratory rate
18
Q

What is a consequence of Acidosis?

A

Sub-optimal Organ Function and eventually cell death (pH=6.8)

19
Q

Which mega principles are implicated in asthma?

A
  • Acidosis -> inc. resp rate

- Hypoxia -> cyanosis

20
Q

Symptoms of Asthma

A

 Wheeze
 Shortness of breath
 Chest tightness
 Cough

The hallmark of asthma is that these symptoms tend to be:
 Variable
 Intermittent
 Worse at night
 Provoked by triggers
 (BTS 2004)
21
Q

What happens to the airway in asthma?

A

Constriction, inflammation and mucus

22
Q

What family are interleukins?

A

A type of cytokine

23
Q

TH2 cells -

AKA?

Type of..?

What do they do?

A

AKA Helper type 2 cells

A type of T cell

They secrete IL-4,5,9,13, 17,25,

Excessive Th2-type responses have been implicated in the development of chronic allergic inflammation and asthma

24
Q

Describe the inflammatory cascade in asthma

A
  • Th2 stimulation (we don’t understand the trigger)
  • Mediator/cytokine/interleukin release
  • Other white cell stimulation
  • Mediator/cytokine/interleukin release
  • Emergence of symptoms of INFLAMMATION and
    asthma (like a mini allergic reaction that is confined to the lungs)
25
Q
  1. Describe the inflammatory cascade in asthma
A
  • Th2 stimulation (we don’t understand the trigger)
  • Mediator/cytokine/interleukin release
  • Other white cell stimulation
  • Mediator/cytokine/interleukin release
  • Emergence of symptoms of INFLAMMATION and
    asthma (like a mini allergic reaction that is confined to the lungs)
26
Q

What do Inflammatory mediators interleukins cause?

A

 obstruction of the smooth muscular walls of the
bronchioles and terminal bronchioles
 oedema of airway mucosa
 increased mucous secretion
 cellular infiltration of the airway walls
 and injury and shedding of the airway epithelium
 This manifests as asthma

27
Q

Characteristics of sputum?

What are they made from?

A
  • Charcot- Leyden Crystals (Bipyramidal crystalloid made from eosinphilic membrane proteins)
  • Curschmann Spiral (spiral-shaped mucus plugs from subepithelial mucous gland ducts and bronchi - from shed epithelium)
28
Q

What type of asthma is covered in this module?

29
Q

What type of asthma is covered in this module?

30
Q

Pathway 2. Atopy / allergy

IgE pathway

A
  • IgE binds to receptor cells on mast cells in the upper
    and lower airways
  • The individual is now referred to as being sensitised
  • On subsequent re-exposure, the allergen to which the individual has been sensitised binds to the IgE causing the mast cells to release inflammatory
    mediators, including histamine and cytokines
  • The resulting pathophysiological response includes
    lung inflammation, oedema, smooth muscle
    contraction and increased mucus production, resulting
    in airway obstruction and eventual lung damage.
31
Q

Pathway 3. Arachidonic Acid

A
  • An additional important mechanism underlying acute asthma involves antigen – antibody interactions resulting in the
    production of Arachidonic acid.
  • Arachidonic acid is a normal fatty constituent of cell
    membranes released following cell injury
  • Arachidonic acid metabolism produces mediators known as
    eicosanoids which are essential for the activation of
    macrophages
  • Arachidonic acid metabolism also results in the promotion of
    vasoactive prostaglandin’s, leucatrines and their mediators
  • All are potent smooth muscle contractors that produce hyper-responsiveness and inflammation
32
Q

3 x pathways in atopic asthma?

A
  • Th2 perspective INFLAMMATION
  • IgE perspective OBSTRUCTION/ALLERGY
  • Arachidonic acid BRONCHO-CONSTRICTION
33
Q

Non-atopic asthma - what is it?

A
  • Non atopic asthma is more commonly seen in adults
    and does not appear to be triggered by any allergens
  • It occurs at unpredictable times, treatment with antiallergen medication has minimal effect and there is
    little or no family history of allergic diseases
  • In some cases the adult has had asthma as a child or
    young adult, which has been quite sever or poorly
    treated, such that their respiratory airways are
    permanently affected
  • Non-Allergic (intrinsic) asthma is triggered by factors not related to
    allergies.
  • Like allergic asthma, non-allergic asthma is characterized by airway
    obstruction and inflammation that is at least partially reversible with
    medication, however symptoms in this type of asthma are NOT associated
    with an allergic reaction.
  • Many of the symptoms of allergic and non-allergic asthma are the same
    (coughing, wheezing, shortness of breath or rapid breathing, and chest
    tightness),
  • But non-allergic asthma is triggered by other factors such as anxiety,
    stress, exercise, cold air, dry air, hyperventilation, smoke, viruses or other
    irritants.

-In non-allergic asthma, the immune system is not involved in the reaction.

34
Q

How can asthma cause cyanosis?

A

Hypoxia due to constriction, inflammation and obstruction by mucus

35
Q

Define central cyanosis

A

Occurs when there is more
than a 5gm/dl of reduced
(deoxygenated) Hb in capillary blood vessels and is usually detectable when the arterial oxygen saturation is less than 85%

36
Q

2 x types of cyanosis

A

Central vs peripheral

37
Q

Normal blood haemoglobin levels

A

Adult male - 14-18gm/dl

Adult female - 12-16 gm/dl

38
Q

Where are beta 1 cells found?

A

Heart and Kidneys

39
Q

Where are beta 2 cells found?

A

liver, lungs, skeletal muscles, uterus, gastrointestinal tract, vascular smooth muscle

40
Q

Where are beta 3 cells found?

A

in fat tissues (could partially explain the obesity - asthma link in F)

41
Q

BTS Guidelines for treatments:

A 
 Short acting B2 agonists
 Inhaled ipratropium bromide
 B2 agonist tablet or syrup
 Theophyllines
 Inhaled steroids
42
Q

3 x lung sounds (quick explanation)

A

Rhonchi - coarse, obstructon of ronchi

Rales - crackle - fluid n alveoli

Wheezing - lungs/alveoli clamped down

Condensed Pathophysiology of Ill-health (15 decks)

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