WK11 - Obstructive Diseases 2 Flashcards

1
Q

Define Asthma

A

A heterogeneous disease, characterised by chronic airway inflammation.

Defined by Hx of Sx: wheeze, SOB, chest tightness and cough where Sx intensity varies over time w expiratory airflow limitations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some causes of Asthma?

A
  • conjunctivitis - blocked tear ducts
  • rhinitis
  • post nasal drip

Kids w asthma also associate with sinitis or rhinitis Tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the prevalence of severe asthma?

A

High intensity Tx (cumulative total 23.5% of asthma pts)

Difficult to treat asthma = poor asthma control + high intensity Tx (17.4%)

Severe refractory asthma = poor asthma control + high intensity Tx + good adh. + correct inhaler technique (3.7%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 asthma phenotypes?

A
  1. Eosinophilic (50%)
  2. Neutrophilic (20-40%)
  3. Ex induced bronchospasm w/o apparent asthma (4-20% but up to 50% in elite athletes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the primary patho mechanism of eosinophilic asthma?

A
  • Type 2 helper cells cytokines (interleukins 4, 5 & 13) induce airway eoinophilia
  • thickening of basement membrane
  • responsive to ICS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the primary patho mechanism of neutrophilic asthma?

A
  • associated w enviro irritants; often severe asthmatics
  • no thickening of basement membrane
  • resistant to ICS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the primary patho mechanism of Ex indcued bronchspasm w/o aparent asthma?

A
  • mast cell release of prostaglandins, leukotrienes and histamines
  • exacerbated by enviro irritants
  • triggered by thermal and oxmotic stress of prolonged hyperventilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is IgE?

A
  • antigen exposure = lymphoid tissue form antibodies
  • attach to mast cells surface in bronchial wall
  • re-exposure to same antigen creates antigen-antibody reaction ot surface of mast cell causing mast cell degranulation
  • release chemical mediators
    (histamine, eosinophils, neutrophils, chemotactic factors leukotrienes, prostaglandins, platelet activating factors)

Given as injection 2/7 - reduces inflammation and prevent hospitalisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does an asthmatic airway look like?

A

Airway smooth muscle:
* hyperresponsiveness
* constriction
* thickening

Sup-epithelial inflammation and fibrosis

Mucus hypersecretion and impaired mucus clearance

Increased eisinophils and/or neutrophils in airway lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some risk factors of asthma?

A

Gender - female 2x more risk
Age - >40y
BMI - >30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is FENO testing?

A

Fractional Exhaled Nitric Oxide
* quick, non-invasive testing - meausres inflammation (irriation/swelling) in airways
* measures how much nitric oxide (parts/billion) is in exhaled air

Does NOT directly test for asthma but can support diagnosis or review if current health plan is working >5y+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How to use a stethoscope to support asthma diagnosis?

A

Listen to lungs - hear wheeze coming from voice body in upp/low chest.
* can be in heard vocal cord dysfunction

If they wheeze too mcuh - may cause dystonia - unable to speak because of inflammation and vocal cord dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some asthma triggers?

A
  • anger, stress
  • pets
  • Ex
  • pollen/bugs in home
  • chemical fumes
  • cold air
  • fungus spores
  • dust
  • smoke
  • strong odors
  • pollution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some EIB considerations?

A
  • can occur during Ex but can be up to 4-6hrs post Ex
  • 2 hypothesis of H2O loss - thermal or osmotic
    Water loss = airway cooling and dehydration.
    Airway injury - role of EIB development and bronchial hyper responsiveness in athletes > healthy.
  • small airways = increased dehydration risk in epithelium

Chronic astmatics - airway smooth muscles exposed to plasma-derived products = contractile muscle properties change = more sensitive/hyper-responsive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Prevention is better than a cure. T or F?

A

TRUE
* short-term basis use of inhaled B2 agonist (SABA or SMART Rx methods)

Long-term - nil Rx to decrease EIB risk.
* ICS and leukotrienes antagonists and 5-lipoxygenease inhibitors - most used –> montelukast

Breathing technique ensure inspried air matches body temp.

Enviro - determine if pt becomes refractory to repeated Ex

Non-pharmacological approaches: masks/scarves in cold, improve CV fitness, training time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Mechanism pathway of EIB.

A
  1. Ex
  2. respiratory water loss
  3. mucosal dehydration
  4. increase osmolarity of airway surface liquid
  5. epithelium + submucosa + presence of increased cellular inflammation
  6. mediator release from cellular inflammation
  7. bronchial smooth muscle sensitivity
  8. bronchical smooth muscle contraction/airway narrowing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What physio. changes are seen with Ex in asthmatic pts?

A
  • > 2/7 bouts of MIPA 8-12wks
  • increase lung function
  • increase asthma control * no change in airway inflammation and SABA use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What did studies on RCT mod vs vig find?

A

Participants have neutrophilic obese-asthma phenotype

1 bout of 45mins MI vs 30mins VI

  • reduced eosinophilic airwya inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does asthma differ from COPD?

A

COPD - chronic continues to progress, irreversible airway changes

Asthma - if controlled Sx decrease, reversible Sx changes.

20
Q

Where do Ex limitations lie?

A
  • ventilatory and gas exchange abnormalities
  • cardiac/respiratory dysfunction and disease
  • skeletal muscle atrophy due to disuse and/or dysfunction
  • Sx: dyspnoea, fatigue and anxiety
21
Q

What is ACOS?

A

Asthma COPD Overlap Syndrome

  • persistent airflow limitation w several features associated with asthma and COPD - clinical pheotypes and mechanisms still unknown
  • may demonstrate fixed airflow obstruction or partial reversibility on spiro test
  • elevated total IgE and slightly increased nitric oxide level
  • Dx of COPD w airway hyper-reactivity and maybe remodelled asthma that has progressed partially reversible or “fixed” airflow obstruction or overlapping COPD/asthma Sx
22
Q

What is bronchiectasis?

A

Children that have had multiple infections as a child.

Repeated infections decreases immune response.

female > male

Between ages of 25-40y, esp. athletes - increased mucus

the “cousin” of CF

23
Q

What is the difference between normal bronchus and bronchiectasis?

A
  • loss of cilia
  • increased mucus
  • destruction of wall
24
Q

What are the benefits of Ex on asthmatics?

A
  • increased Ex capacity
  • increased muscle strength
  • increased QoL
  • decreased dyspnoea
  • health care utilisation benefits
  • psychosocial benefits
  • benefits other chronic respiratory diseases too
25
Q

Define Pulmonary rehab?

A

An evidence-based, multidisciplinary and comprehensive intervention ofr pts w chronic respiratory disease who are symptomatic and decreased ADLs

Reduces Sx, optimise fucntional status, increase participation and reduce health care costs through stabilising/reversing systemic manifestations of disease.

26
Q

What is the inclusion criteria?

A
  • Sx of breathlessness, fatigue or low PA lvl
  • a confirmed respiratory conditions
  • recovering from acute exacerbation
  • group environment
  • intact cognition
  • independtly mobile (can have mobility aids)
  • current smoking can attend to aid in quitting
  • can come if O2 dependent
27
Q

What is the exclusion criteria?

A
  • severe cognitive impairment
  • severe psychotic disturbance
  • relevant infectious disease
  • MSK/neuro disorders that prevent Ex
  • unstable CVD (unstable angina, aortic valve disease, unstable PHTN.
  • known metabolic cancers
28
Q

What are the Ex program benefits?

A
  • improve QoL
  • Improve breathlessness and fatigue
  • central desensitisation to dyspnoea
  • reduce dynamic hyperinflation
  • improve MSK function
  • improve Ex ability
  • changes measured by 6MWT
  • no RCT’s have Ax anxiety/depression effect

Benefits following PRP no longer clear at 6M following program completion w/o maintenance programs

29
Q

What is included in the pt Ax?

A
  • Med Hx
  • dyspnoea Ax
  • nutritional status
  • smoking Hx
  • Ax MH - K10
  • QoL - SGRQ (preferred)
  • functional/Ex capacity Ax
  • postural Ax
30
Q

What to ask in Med Hx?

A
  • definitive Dx?
  • comobidities
  • respiratory illness Hx - exacerbations, hospitalisations
  • med list (including O2 Px)
  • Ax dyspnoea lvl - MRC, modified med research council, RPD, dyspnoea 12
  • radiological - full RFT’s incl. diffusion capacity, CT chest, CXR, ABGs, ECG, echo, FENO testing
  • bloods - determnie physio. and biochemical states: disease, mineral content, pharmaceutical drug effectiveness, organ function

“BODE”
* BMI
* Obstruction
* MMRC
* Ex tolerance

31
Q

What are some considerations for nutrition and smoking?

A

BMI <20 = underweight
* poor nutritional status implicated in higher mortality
* poor blanace w energy demands

BMI >30 = overweight
* affects abdominal/thoracic pressure

Recent Hx of Wt loss?
* >10% in last 6/12 or 5% in 1/12

Smoking
* largest risk factor of COPD
* decrease Hb O2 carrying capacity - affect SPO2 lbls
* expired CO monitoring

32
Q

What are some tools for Ax QoL and MH?

A

K10; HADS-D/A; PHQ4/9

Disease specific…
* St George’s Respiratory Questionnaire
* Chronic Respiratory Questionnaire
* Juniper - ACQ
* Tautons
* CAT

33
Q

What are some MH comorbidities w Pulmonary Conditions?

A
  • distress / coping strategies
  • anxiety, depression
  • panic attacks
  • PTSD
34
Q

How long does PRP effects last and improve health care utilisation?

A

Weekly un/supervised maintenance Ex can increase effects up to 12M got mild to mod obstructive conditions

Mild COPD and asthmatic, it is more likely 9M

Comunity based maintenance Ex
* Pts must complete PRP in prevous 12/12
* Practitioner will have completed program and linked with local program for mentoring
* cost and access = barriers

35
Q

What are endobronchial valves?

A

Valves are put in the bronchial - bronchoscopy
Tube is placed down their throat into their lungs.

The valve acts as a lung reception to prevent the lung from collapsing to ensure airflow is intact.

36
Q

What is lung lobectomy?

A

Lung surgical resection: lung volume reduction options
* early stages of NSCLC (<III)
* lung disease - bullous emphysema
* lung tumour
* infection - tuberculosis
* dilated bronchi of bronchiectasis
* lung abscess
* atelectasis

37
Q

How many lobes does each lung have?

A

L lobe has 2, smaller as it must accommodate space for heart

R lobe has 3 and is bigger

38
Q

What are the types of lobectomy procedures?

A
  1. Open - lobe removed through long chest incision
  2. VATS - love removed with assistance of instrucments and camera
  3. RATS - love removed with assistance of robots
39
Q

What are the thoracotomy “lung transplant” guidelines?

A

Must participate in pulmonary rehab!

40
Q

What is the QLD lung and heart transplant Ax pathway?

A
  • initial Ax - surgeons and multi-D team
  • investigations
  • follow up med team Ax - refer to locak respira team
  • in patient TCPH stay 4/7 - RHC, stress, MRI, bronchoscopy, cancer screening, vascular Ax, metabolic challenge testing
  • Ax of qualifying requirements
  • listing
41
Q

What to look ofr in quadricep strength testing?

A
  • loss of peripheral skeletal muscle = poorer prognosis
  • increased SOBOE, reduced ET, worsening HQoL
  • Quadriceps Score corrected for BW (%QS)
  • Handhelp dynamo. w adjustable strap to measure maximal knee ext for 4s
  • procol - 3 x 4 s each leg w min. 1-2/60 rest
42
Q

What are the causes of lung cancer and how is it diagnosed?

A
  • smoking
  • occupation exposure
  • pollution
  • genetics

Dx
* often Dx late - Sx vague. No routine screening in Aus for early detection

43
Q

What are the Sx of lung cancer?

A
  • cough - new, persistance, changed
  • coughing up blood
  • fatigue
  • wt loss
  • chest pain
  • breathlessness
  • voice hoarseness
44
Q

What is the Tx of lung cancer?

A
  • targeted therapies
  • immunotherapy
  • radiotherapy
  • chemotherapy
  • surgery

Aim to extend life and improve QoL

45
Q

What is the diff between local and systemic Tx for lung cancer?

A

Local
* treat tumours where they originate, do not treat cells that have spread - surgery and radiation

Systemic
* treat cancer cells wherever in body - chemo, targeted therapies, immunotherapy

46
Q

What is sputum?

A

“Mucus” - secretions normally produced by cells that line airwyas

  • purpose is to remove unecessary cells and debris from lungs
  • may contain pus, blood or other debris - causing colour change
  • volume of sputum produced varies on lung condition and whether infection is present