Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

osce prep > respiratory (asthma, copd) > Flashcards

respiratory (asthma, copd) Flashcards

1
Q

how would you describe what asthma is

A

asthma is an chronic inflammatory airway disease characterised by intermittent reversible airway obstruction

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

what is the pathophysiology of asthma

A

*ACh is involved in bronchoconstriction vs NO is involved in bronchodilation

airway hyperresponsiveness
- variable component: acute inflammatory events that release mediators which triggers cholinergic pathways that lead to release of ACh, ACh binds to muscarinic receptors on airway smooth muscle cells to cause vasoconstriction
- chronic component: chronic inflammation leads to structural and phenotypic changes leading to hyperplasia (increase amount) and hypertrophy (increase size) of airway smooth muscle cells

airway remodelling
- allergen leads to immune system activation and amplification
- release of paracrine signals that causes proliferation of cells by epithelial and immune cells
- triggers mesenchymal cells (fibroblasts and airway smooth muscle cells)
- increase mass and thickness of airway smooth muscles
- leads to narrowing of lumen and increases in airway resistance

airway inflammation
- allergen involves IgE allergic response whereby allergen is presented to allergen presenting cell - dendritic cell which presents it to TH2 cells and activates the immune system in releasing immune cells like mast cells, eosinophills, T lymphocytes that release inflammatory mediators like leukotrienes, histamine, prostaglandin and cytokines
- B cells are also activated, leading to antibody production including IgE, causing further activation of mast cells by IgE
- inflammatory mediators causes bronchoconstriction and excessive mucus secretion
- overall leading to airway obstruction

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

what is the clinical symptoms of asthma

A
  • breathlessness
  • chest tightness
  • coughing (that worsens at night or early morning)
  • wheezing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the risk factors of asthma

A

host factors
- genetics
- gender (M > F)
- obesity

environmental factors
- allergens (indoor/ outdoor)
- occupational sensitizers
- air pollution
- tobacco smoke
- respiratory infections
- socio-economic factors

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

what are the factors that can cause asthma exacerbations

A
  • allergens
  • respiratory infections
  • exercise and hyperventillation
  • weather changes
  • air pollution
  • occupational sensitizers
  • food and additives
  • drugs
  • GERD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is exercise induced bronchoconstriction

A

acute narrowing of airways in lungs triggered by exercise, defined as a decrease in FEV1 by 10% or more from pre-exercise value

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how is asthma assessed and diagnosed

A
  1. hx of symptom pattern
    increased asthma probability
    - classic triad
    - worse at night or early morning
    - variable over time and in intensity
    - triggered by infections, allergens, pollutants, weather changes, exercise, strong smells, smoke and irritants

decreased ashtma probability
- isolated cough with no other respiratory symptoms
- chest pain
- chronic sputum production
- shortness of breath associated with dizziness or lightheadedness or peripheral tingling
- exercise induced dyspnea with noisy inspiration

  1. evidence of variable airflow limitation
    - confirm presence of airflow limitation (document decrease in FEV1/FVC)
    - confirm variation in lung function greater than in healthy (using spirometry to compare FEV1 before using dilator vs 15-20mins after to determine excessive bronchodilator reversibility for diagnosis; peak flow meter is used for peak expiratory flow monitoring)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the normal FEV1/FVC ratio

A

> 0.75-0.80 in healthy adults
0.90 in children

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

what does FEV1 measure

A

measures volume of air exhaled forcefully in first second of maximal expiration

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

what does FVC measure

A

maximum amount of air that can be exhaled when blowing out as fast as possible after full inspiration

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

what does the FEV1/FVC ratio measure

A

measures the proportion of FVC that can be exhaled in first second of forced expiration

differentiates between obstructive and restrictive disease (FEV1/FVC decreases in obstructive disease but FEV1/FVC ratio may be maintained in normal range or even increased for restrictive disease as both FEV1 and FVC decreases)

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

what are the non-pharmacological management of asthma

A
  • avoidance of tobacco smoke
  • increase physical activity (general health benefits and advice on how to manage exercise induced bronchoconstriction)
  • occupational asthma
  • dealing with emotional stress through relaxation strategies
  • breathing exercises
  • vaccinations
  • avoiding medications like NSAIDs and BB
  • sublingual immunotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the goals of therapy of asthma

A
  • symptom control: achieve good control of symptoms and maintain normal activity level
  • risk reduction: minimise future risks of asthma-related mortality, exacerbations, persistent airflow limitation and s/e
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the pharmacological management for asthma

A

reliever
- SABA
- ICS-formoterol
- SAMA (less frequently used)

controller
- ICS
- ICS-formoterol
- ICS-LABA
- LTRA
- LAMA (used less frequently)

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

what are the benefits of long term use of corticosteroids

A
  • most effective anti-inflammatory medication for persistent asthma
  • reduce asthma symptoms
  • reduce use of reliever
  • improve QoL
  • improve lung function
  • control airway inflammation
  • reduce airway hyperresponsiveness
  • reduce frequency and severity of exacerbations
  • reduce asthma mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the s/e of corticosteroids

A

inhaled
- cough, dysphonia, oral thrush

systemic
- osteoporosis, skin thinning, immunosuppression, easy bruising, HTN, DM, muscle weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the s/e of beta agonists

A
  • tachycardia, palpitation, HA, tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the s/e of montelukast

A
  • N, HA, neuropsychiatric events (depression, agitation, insomnia, suicidal, restlessness)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the s/e of LAMA

A
  • dry mouth
20
Q

what are the s/e of theophylline

A
  • GI: N/V
  • CNS: insomnia, HA, seizures
  • CV: flutter, tachycardia
21
Q

how to manage asthma exacerbations

A
  1. initial assessment (ABC: airway, breathing, circulation)
  2. further triage by clinical status
  3. assess clinical progress frequently and measure lung function in all patients 1hr after initial treatment (discharge if FEV1 or PEF is 60-80%; continue treatment and assess frequently if FEV1 or PEF <60%)
22
Q

how to further triage by clinical status

A

mild-moderate if
- talks in phrases
- prefers sitting or lying
- not agitated
- RR increased
- accessory muscles not used
- O2 saturation >90-95%
- PR 100-120
PEF >50%

manage with SABA, ipatropium (consider combi of both), short course OCS to speed up recovery

severe if
- talks in words
- sits hunched forward
- agitated
- RR >20
- accessory muscles used
- PR >120
- O2 saturation<90%
- PEF 50% or less

manage with SABA, ipatropium, IV/PO corticosteroids, consider IV magnesium

23
Q

what is the follow-up and monitoring duration for asthma

A
  • exacerbations TCU in 1w
  • monitoring TCU 1-3m after initiation, q3-12m after
24
Q

what is part of a written asthma plan

A
  • asthma triggers
  • medications (reliever, controller, administration techniques, for other comorbs)
  • symptom monitoring (signs of well-controlled vs warning signs)
  • emergency action plan for exacerbations (use of reliever, when to contact HCP or emergency care)
  • follow ups
25
Q

how would you explain what is copd

A

copd is a chronic inflammatory lung disease characterised by progressive, largely irreversible airway obstruction

26
Q

what are the risk factors of copd

A
  • smoking
  • environmental tobacco smoke
  • hx of TB
  • occupational hazards
  • exposure to biomass burning
  • alpha1-antitrypsin deficiency
27
Q

what are the main pathological features

A
  • obstructive bronchiolitis, fibrosis
  • emphysema (alveolar wall destruction)
  • chronic bronchitis, mucus hypersecretion
28
Q

what is the pathophysiology of copd

A

obstructive bronchiolitis, fibrosis
- smoke and irritants interact with epithelial cells which triggers release of profibrotic mediator (a growth factor) that acts of fibroblast to produce matrix protein leading to peribronchiolar fibrosis (scarring of tissue)
- structural change results in narrowing of small airways thus obstructive bronchiolitis

emphysema (alveolar wall destruction)
- imbalance between protease and anti-protease activity
- irritants trigger activation of immune system
- neutrophils and macrophages release protease like neutrophil elastase and MMP9 that causes break down of elastic fibers important for alveoli attachment that hold airway open

chronic bronchitis, mucus hypersecretion
- goblet cell hyperplasia
- mucosal edema
- mucus hypersecretion
- proteases produced by macrophages also involved in mucus production and causes a build up of mucus

air trapping
- attributed to premature closure of small airways upon expiration due to fixed narrowing of airways resulting from fibrosis, mucus hypersecretion and loss of alveolar attachments
- can cause lung hyperinflation and dynamic hyperinflation (leading to reduced exercise tolerance as next inhale starts before fully exhaling)
- already hypoxemia (low PO2) due to airway narrowing and obstruction, but air trapping reduces volume of CO2 escaping thus causing hypercapria (increased PCO2) but partial pressures of gases important for gas exchange via diffusion and major changes will affect efficient gas exchange in airways

oxidative stress
- mainly mediated by ROS
- ROS increases inflammation and contribute to bronchitis and bronchiolitis
- worsens tissue damage and causes copd progression

29
Q

compare asthma with copd

A

age of onset
- asthma: any age but usually childhood
- copd: >40yo

patterns of sx
- asthma: shortness of breath, wheezing, cough, chest tightness; variable; worse at night or early morning
- copd: dyspnea, chronic cough, sputum; usually continuous

hx
- asthma: allergies, personal hx of childhood asthma/ FHx
- copd: exposure to risk factors

lung function
- asthma: variable airflow limitation, may be normal between sx
- copd: persistent airflow limitation (FEV1/FVC <0.7)

chest xray
- asthma: normal
- copd: severe hyperinflation

time course
- asthma: no worsening over time, may improve spontaneously
- copd: slowly worsen over time (years), sx improve with treatment but progression is usual

30
Q

how is copd assessed

A

using spirometry
GOLD 1 (mild): FEV1 ≥80%
GOLD 2 (moderate): 50% ≤ FEV1 <80%
GOLD 3 (severe): 30% ≤FEV1<50%
GOLD 4 (very severe): FEV1<30%

based on symptoms (mMRC questionnaire)
0 (none) if only breathlessness with strenuous exercise
1 (mild) if SOB when hurrying or walking up a slight hill
2 (moderate) if walks slower than age group or has to stop for breath when walking on level ground at own pace
3 (severe) if stops for breath after walking 100m or a few minutes on level ground
4 (very severe) if breathless when dressing/ undressing or too breathless to leave the house

symptoms also can be assessed based on CAT assessment, an 8 item measure of health status impairment in COPD

31
Q

what is the classification of copd

A

A (less sx, low risk) if GOLD1-2 and mMRC 0-1 or CAT<10
B (more sx, low risk( if GOLD 1-2 and mMRC 2-4 or CAT ≥10
C (less sx, high risk) if GOLD 3-4 and mMRC 0-1 or CAT <10
D (high sx, high risk) if GOLD 3-4 and mMRC 2-4 or CAT ≥10

32
Q

what is a copd exacerbation

A

an acute worsening of respiratory symptoms that result in additional therapy, classified as high risk and low risk

high risk if ≥2 exacerbations in the past 1 yr or ≥1 leading to admission
low risk if 0/1 exacerbation but not leading to admission

33
Q

what are the goals of therapy of copd

A
  • reduce symptoms (relieve symptoms, improve exercise tolerance, improve health status)
  • reduce risk of exacerbations (prevent disease progression, prevent and treat exacerbations, reduce mortality)
34
Q

what is the pharmacological management of copd

A

SABA
- salbutamol
LABA
- indacaterol
- formoterol
- olodaterol

SAMA
- ipatropium
LAMA
- tiotropium
- glycopyrronium
- umeclidinium

ICS-LABA
- budesonide/formoterol
- fluticasone/salmeterol
- fluticasone/vilanterol

LAMA-LABA
- umeclidinium/vilanterol
- glycopyrronium/indacaterol
- tiotropium/olodaterol

ICS
METHYL XANTHINES (theophylline)
PDE4i
ABX (azithromycin)

35
Q

what is the GOLD’s recommended initial pharmacotherapy for each classification of copd

A

A: SAMA/SABA
B: LAMA/LABA (LAMA>LABA)
C: LAMA
D: LAMA or LAMA-LABA or ICS-LABA

36
Q

what is the non-pharmacological management of copd

A
  • reduce exposure to risk factors including smoking cessation
  • vaccination (flu, pneumococcal, pertussis)
  • self-management on breathlessness, energy conservation and stress management
  • written action plan
  • increase physical activity
  • oxygen therapy
  • end of life care
  • pulmonary rehab (patient education, exercise training, nutritional support, psychosocial support)
  • surgery
37
Q

what does the written action plan comprise of

A
  • severity
  • medications
  • symptom monitoring
  • smoking cessation (if applicable)
  • pulmonary rehab programme (if applicable)
  • breathlessness, energy preservation and relaxation techniques
  • exacerbation management (avoidance of aggravating factors, contact number in the event of an exacerbation)
38
Q

what is the follow up for copd

A

based on
dyspnea
- LABA/LAMA –> LABA+LAMA –> consider switching inhaler device and identifying and treating other causes of dyspnea
- LABA+ICS –> LABA+LAMA+ICS –> consider switching inhaler device and identifying and treating other causes of dyspnea (or trying LABA+LAMA)

and exacerbation
- LABA/ LAMA –> LABA+LAMA –> (if eos ≥100cells/µ, else skip) ICS+LABA+LAMA –> azithromycin (esp in ex smokers)
- LABA/LAMA –> ICS+LABA –> LABA+LAMA or ICS+LABA+LAMA –> azithromycin (esp in ex smokers)

39
Q

what are the criterias that support use of ICS

A
  • exacerbation leading to hospitalisation
  • ≥2 exacerbations/ year
  • eos ≥300cells/µL (indicates esosinophil inflamm)
  • hx of concom asthma
40
Q

what are the criterias supporting the use of triple therapy

A
  • severely symptomatic
  • moderate to very severe airway obstruction
  • history of frequent and/or severe exacerbations
41
Q

what is the presentation of an exacerbation

A
  • increase sputum production
  • worsening dyspnea
  • worsening cough
  • drowsiness
  • fatigue
  • decreased exercise tolerance
42
Q

what are the 5 As of smoking cessation

A
  • ask about use of tobacco
  • advise to quit
  • assess willingness and rationale
  • assist in quitting
  • arrange for follow-up
43
Q

what are the vaccinations

A
  • influenza
  • pneumococcal (PCV13, PPSV23)
  • Tdap
  • COVID19
43
Q

what are the components of pulmonary rehabilitation

A
  • patient education about disease and treatment options
  • exercise training
  • nutritional support
  • psychosocial support
44
Q

what are the differential diagnosis for copd exacerbations

A
  • pneumonia (chest radiograph, assess CRP and/or procalcitonin)
  • pneumothorax (chest radiograph/ ultrasound)
  • pleural effusion ie. water buildup in lungs (chest radiograph/ ultrasound)
45
Q

what is the goal of therapy for copd exacerbations

A
  • minimise impact of current exacerbation
  • prevent development of subsequent exacerbations
46
Q

what is the management of copd exacerbations

A
  • SAMA (combi with BA as first line)
  • SABA
  • oxygen therapy
  • vitamin D supplement for severe vitD deficiency of <10ng/ml
  • OCS (prednisolone) x5d
  • abx (augmentin, macrolide, cefuroxime, FQ) *controversial use
  • respiratory support

osce prep (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions