Brainscape's Knowledge GenomeTM

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


See full index

Respiratory > Asthma, CF, bronchiectasis > Flashcards

Asthma, CF, bronchiectasis Flashcards

1
Q

How do you check for bronchial hyperresponsiveness in asthma?

A

Bronchial challenge test

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

When may it be appropriate to check for bronchial hyperresponsiveness in asthma?

A

If clinical features are atypical or where the dx has important implications (defence force employment, athletes)

Unnecessary if variable airflow obstruction has already been documented

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

What does a high serum eosinophil count in asthma suggest?

A

Likely to be responsive to ICS or monoclonal ab

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

What does a high exhaled nitric oxide level mean in asthma?

A

Allergic inflammation

Likely to respond to steroids

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

What’s Samter’s triad?

A

Asthma
Aspirin intolerance - triggers asthma
Nasal polyps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does allergic bronchial pulmonary aspergillus (ABPA) present?

A 
Difficult to control asthma
Recurrent pulmonary infiltrates
Recurrent infections not responsive to abx 
Bronchiectasis with thick sputum
Very high IgE (>1000IU/ml)
Evidence of aspergillus hypersensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is allergic bronchial pulmonary aspergillus (ABPA)?

A

Hypersensitivity response to the fungus, aspergillus

Occurs in asthma and CF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Rx allergic bronchial pulmonary aspergillus (ABPA)

A

Steroids

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

How does eosinophilic granulomatosis with polyangiitis (EGPA) present?

A

Symptoms vary from mild to life threatening

But almost everyone has asthma +/- nasal polyps and high eosinophils

Multi-organ disease - peripheral neuropathy, mononeuritis multiplex, skin disease, cardiac disease

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

Rx eosinophilic granulomatosis with polyangiitis (EGPA)

A

Steroids
MTX, mycophenolate, cyclophosphamide
Mepolizumab (reduce eosinophils)

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

Explain the stepwise management of asthma

A

Step 1
ICS-fomoterol PRN

Step 2
Daily ICS-fomoterol + PRN same

Step 3
Daily low dose ICS-LABA + PRN SABA

Step 4
Daily medium dose ICS-LABA + PRN SABA

Step 5
Daily high dose ICS-LABA +/- add on therapy + PRN SABA

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

What are some potential add on therapies in severe asthma?

A

Tiotropium - useful in frequent exacerbations, airflow obstruction
Macrolides (azithromycin) - useful in frequent exacerbations, cough + sputum
Montelukast - useful in aspirin sensitive
Monoclonal abs - useful in frequent exacerbations

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

When is omalizumab indicated in asthma?

A

Targets IgE
Allergic asthma
Used in addition to ICS + LABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When are mepolizumab and benralizumab used in asthma?

A

Targets IL5

Eosinophilic asthma

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

What is bronchiectasis?

A

Permanent dilation of bronchi and bronchioles due to destruction of airway muscles and elastic connective tissue

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

Causes of bronchiectasis

A
  • Post-infectious (e.g. pertussis)
  • ABPA
  • COPD
  • Traction secondary to fibrosis (radiological dx)
  • Aspiration
  • Obstruction
  • Immunological defects (primary, secondary)
  • Congenital defects (Marfan’s, ciliary defects, A1AT deficiency)
  • Inflammatory - RA, coeliac disease, SLE, IBD
  • Young’s syndrome
  • Amyloidosis
  • CF

Exacerbating comorbidities: GORD/aspiration, non-tuberculous mycobacterium, sinus disease

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

Investigations in bronchiectasis

A
  • CT chest - look for tree and bud and granulomatous nodules - might indicate non-tuberculous mycobacterium
  • Sputum x3 - AFB to look for non-tuberculous mycobacterium
  • ABPA - IgE and aspergillus precipitants
  • Immunoglobulins - if isolated level of IgG, can receive IV gammaglobulins which can reduce exacerbations
  • 6MWT
  • ABGs

Consider

  • CF genotyping
  • ECHO
  • Bronchoscopy
  • Immune test including HIV
  • Nasal brushings to exclude coeliac syndrome
  • Gastroscopy to exclude GORD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the organisms commonly implicated in bronchiectasis?

A
  • Pseudomonas - important player. Very hard to eradicate.
  • Non-tuberculous mycobacterium
  • Aspergillus
  • Stenotrophomonas nalophilia
  • Staph aureus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Rx bronchiectasis

A
  • Treat the cause
  • Improve airway clearance/chest physio/pulmonary rehab
  • Treat infection (acute and chronic) - PO ciprofloxacin or IV beta-lactam +/- aminoglycoside
  • Treat airway obstruction - salbutamol +/- ICS. 2nd line ICS/LABA, theophylline, tiotropium.
  • Treat chronic inflammation - erythromycin, azithromycin. 2nd line doxycycline. 3rd line nebulised tobramycin.
  • Inhaled hypertonic saline - can be trialled in frequent exacerbators or has significant symptoms due to viscous mucous (be careful if FEV<1L due to bronchospasm)

Less common

  • Surgical resection
  • Lung transplant
  • Bronchial artery embolization for significant haemoptysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What must you monitor if using macrolides long-term for bronchiectasis?

A

Monitor sputum for resistance and increased non-tuberculous mycobacterium
Monitor ECG for prolonged QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pathophysiology of CF

A

Defect in the cystic fibrosis transmembrane conductance regulator (CFTR)

CFTR is blocked in CF –> can’t transport Cl out of cell –> Enac tries to compensate by transporting Na into cell to neutralise Cl –> dehydrated airways + viscous mucous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the 6 functional classifications of CFTR mutations?

A

1) No protein
2) No traffic (most common phenotype due to homozygous DF508 genotype)
3) No function (gate doesn’t open properly) due to G551D genotype
4) Less function
5) Less protein (minor abnormality)
6) Less stable (minor abnormality)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is CF diagnosed?

A

1) Meconium ileus at birth
2) Heal prick test - high sensitive, low specificity
3) Sweat test - chloride >60mmol/L, borderline 40-60mmol/L
4) Gene testing - 50 panel test; but >2000 mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does CF affect the lungs?

A

CFTR protein defect –> unable to secrete chloride –> sodium follows and stays inside cell –> thick secretions –> infection –> inflammation –> bronchiectasis –> lung destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Treatment options for CF

A

1) CFTR modulators
Ivacaftor - CFTR potentiator - opens the channel of the protein

Tezacaftor - CFTR corrector - moves the protein onto the cell surface

Elexacaftor - CFTR corrector - moves the protein onto the cell surface

Different combinations available for homozygous/heterozygous DF508 mutations
Ivacaftor available for G551D mutations

Improves FEV1 and reduces exacerbation

2) Inhaled DNase
- Improves FEV1

3) Azithromycin
4) Inhaled abx - tobramycin, colistin

4) Inhaled mucolytics - hypertonic saline, mannitol
- Improves FEV1

5) Inhaled bronchodilators
6) Lung transplant (less common now)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Common pathogens in CF

1) Children
2) Adults

A

1) Staph aureus

2) Haemophilus, pseudomonas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Why is it important to treat pseudomonas colonisation aggressively in children with CF?

A

To prevent chronic infection due to its ability to cause resistance, form mature biofilms which makes it hard for abx to penetrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are some strategies to get rid of pseudomonas colonisation?

A

Long-term oral abx
Long-term nebulised abx
Airway clearance
?Inhaled DNAse to break up biofilms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the 2 types of non-tuberculous mycobacterium often seen in CF?

A

1) MAC
- Usually seen in older people
- Mild disease

2) Mycobacterium abscessus
- More advanced disease with a rapid decline in lung function
- Active infection is contraindicated in transplant

Clinical guidelines suggest annual screening for NTM

Even if NTM is grown in sputum culture, it does not mean there is NTM lung disease. Most people with single positive culture will not require treatment. The decision to treat will depend on symptoms, or when there is a lack of response to treatment of typical CF infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Rx non-tuberculous mycobacteria in CF

A

Very difficult!!
Often resistant to abx.

Will usually require 3 abx for 12 months+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Clinical features of CF (other than lungs)

A

1) Pancreatic insufficiency (90% will have this)
- Due to thickened pancreatic secretions –> activation of proteolytic enzyme –> autodigestion
- Most will require pancreatic enzymes for life

2) GI
- Meconium ileus (neonate)
- Distal intestinal obstruction syndrome (adults) - thick secretions block the ileo-caecal junction. May present with faecal mass in RIF mimicking appendicitis. Rx colonlytely, gastrograffin, may require laparotomy
- GORD
- Rectal prolapse
- Intussusception

3) Bone disease
- Dexa every 2 years
- Rx: calcium, vitamin D, bisphosphonates

4) Infertility
- Males: absent vas deferns
- Females: can generally conceive but may have dehydrated secretions –> fallopian tube adhesions, slow passage of oocyte to uterus

5) Mental health

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What’s a bronchial provocation challenge?

A

Gold standard for asthma diagnosis. Picks up bronchial hyperresponsiveness.
- Gets done when RFTs are inconclusive but symptoms are suggestive of asthma

DIRECT challenge
Deliver noxious stimuli that acts on SM receptors (histamine and methacholine)
Positive test: 21% fall in FEV1 
Sensitive but not specific 
Lots of false positives

OSMOTIC INDIRECT challenge
Detect the presence of inflammatory cells in the airways
Hypertonic saline, exercise and mannitol
Positive is 15% or more reduction in FEV1
More specific but not sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What’s cardiopulmonary exercise testing?

A

Do it on bicycle or treadmill
Cardiac, pulmonary and muscle assessment
Work patients to target HR or workload

For people with SOB with unknown cause
Also done pre-pneumectomy to determine suitability

Measures
VO2 (ability to extract oxygen by the muscle; increases lineally with workload; good sign of physical fitness or functional aerobic capacity; VO2 can go up as you get fitter; HR drops as you go fitter)
VCO2
Minute ventilation (VE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What’s your maximum heart rate?

A

Age-30

HR is the most important physiological change which contributes to decline in VO2 with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What’s maximal voluntary ventilation?

A

FEV1 x 40

We all have ventilatory reserve but having lung disease reduces the maximum voluntary ventilation

36
Q

2 types of bronchiectasis

A

Focal
One lobe only

Diffuse
More than one lobe

37
Q

Causes of focal bronchiectasis

A

Something is blocking or narrowing a specific airway
But not lung ca - grow too quickly to develop bronchiectasis

Foreign body
Slowly growing tumour
Lymphadenopathy
Twisting or displacement of airways after a lobar resection

38
Q

Next best test for focal bronchiectasis

A

Bronchoscopy

Looking for the endoluminal problem that is contributing to the bronchoscopy

39
Q

Causes of diffuse bronchiectasis

A

Infections

  • Postviral (adenovirus, measles, influenza, pertussis, varicella, HIV)
  • Mycobacterium
  • ABPA
  • Severe bacterial infections

Congenital conditions
- CF

Immunodeficiency conditions
- CVID

Rheumatological conditions
- 30% RA have bronchiectasis

Toxin or drug exposure
- Chlorine inhalation

40
Q

Diffuse bronchiectasis involving upper lobe

DDx

A

CF

ABPA

41
Q

Sinus disease (bad) and bronchiectasis
Loss of sense of smell
Young person

A

Primary ciliary dyskinesia

42
Q

Primary ciliary dyskinesia
What is it?
Diagnosis

A

Autosomal recessive
Variable penetrance
Absent cilia (extreme; dexta cardia) or shortened cilia or cilia that don’t move properly

Ciliary motility study - nasal swab with microscope to look at cilia and their movements

Or sometimes diagnosed in sinus surgery

43
Q

Primary ciliary dyskinsia

Clinical features

A

Sinusitis is way more severe than bronchiectasis

Recurrent OM in adults!!

Compared to CF - bronchiectasis disease is equal to sinus disease

44
Q

When do you suspect CF in adults with bronchiectasis?

A

Age <40
Upper lobe disease
FHx of recurrent chest infections/CF
S.aureus in sputum

45
Q

Diagnosis of CF in suspected adults

A

CF genetic panel (as the genetic abnormalities are mild)

Not the sweat test

46
Q

Conditions associated with bronchiectasis

A 
Primary hypogammaglobulinaemia 
CLL 
Myeloma
Chemotherapy
All cause low IgG --> can result in bronchiectasis

Rheum
RA
SLE
Sjogren’s

47
Q

MANAGEMENT bronchiectasis

A

Sputum clearance techniques

  • PEP device
  • No postural drainage due to reflux risk for adults

Treat acute exacerbations

  • Volume change, colour change
  • Treat for 2 weeks
Suppress microbial load 
- Prophylaxis
- Rules
#Bronchiectasis
#Pseudomonas
#2 or more chest infections/year
- Oral macrolides (antiinflammatory effects, reduce sputum volume, inhibit biofilm layer, colony forming units) or nebulised aminoglycosides (gentamycin or tobramycin)

Treat underlying condition
E.g. immunoglobulin therapy for low IgG

Reduce excessive inflammatory response
- Consider ICS for obstructive picture/reversibility

Control bronchial haemorrhage

Surgical removal of segments/lobes

48
Q

One test to do in bronchiectasis

A

Sputum MCS
Look for pseudomonas - damaging to the airways and make the disease progress

This is a gamechanger

49
Q

Asthma severity is defined by

A

Control

NOT lung function

50
Q

Difficult to treat asthma is

A

those remained uncontrolled with high dose ICS

51
Q

Severe asthma is

A

Subset of difficult to control asthma

Asthma that remains uncontrolled despite high dose ICS + LABA + leukotriene modifier or theophylline for the previous year OR

Treatment with oral corticosteroid for at least half the previous year

OR asthma that requires such treatment in order to remain well controlled

52
Q

4 questions to ask to assess control of asthma

A

1) Day time symptoms
2) Need for reliever
3) Limitation of activity
4) Sx at night or on waking in the middle of the night

0 = good control
1-2 = partial control
3 = poor control
53
Q

Reasons for poor control asthma

A 
RSV
Influenza
Beta blockers even eyedrops
NSAIDs
Chinese medicine
Dust mites
Mould
Mouldy hay (aspergillus loves this - Farmer's lung, interstitial pneumonitis)
Thunderstorm asthma
Canola 
URT inflammation - allergic rhinitis
GORD

Less common
CF
ABPA
EGPA

54
Q

Treatment mild asthma

A

Minimal symptoms
Well controlled of low dose ICS

Need treatment = remodelling of airways

Must have low dose ICS to prevent exacerbation (people who died from thunderstorm asthma were either not on ICS cause symptoms were mild or were not compliant with their ICS)

55
Q

Treatment difficult to treat and severe asthma

A

High dose ICS/LABA

Others
Tiotropium in severe asthma
Macrolides (antiinflammatory)
LT modifier (montelukast) - use only in aspirin related asthma and polyps

Biologics

  • Must fulfil clinical, medication and investigation criteria
  • Poorly controlled asthma and mainly in eosinophilic allergy phenotypes
  • Works extremely well
  • Omalizumab (anti IgE)
  • Mepolizumab (anti-IL5)
  • Benzalizumab (anti-IL5)
  • Dupilimab (anti-IL4)

Theophylline - not recommended anymore

56
Q

Types of asbestos

A

Horrible fiber and brilliant insulator

Blue more likely to cause mesothelioma

57
Q

How long from exposure to asbestos related lung disease?

A

Latency period if long between exposure and development of asbestos related lung disease (often 30-40 years)

58
Q

5 types of asbestos related lung disease

A 
Pleural plaques
Asbestos related pleural disease
Asbestosis
Mesothelioma
Lung cancer (NSCLC, squamous cell)
59
Q

Pleural plaques are

A

Calcium forming asbestos fibers

Benign
NOT premalignant 
Asymptomatic 
Can't affect lung function 
Marker of asbestos exposure
60
Q

Asbestos related pleural disease

A

Diffuse pleural disease
More than 25% circumference showing pleural disease
Benign
NOT pre malignant

Can cause symptoms if there is enough circumference involved causing restrictive process

61
Q

Rounded atelectasis

A

Pleural wrapping around normal lung
Can look like lung mass

Must be immediately adjacent to pleura

Need to have other evidence of asbestos related pleural disease (>25% circumference involvement)

Crows feet (lines around the mass)

May not even need biopsy if very characteristic on CT

62
Q

Asbestosis

A

Interstitial lung disease associated with asbestos

Requires to the most prolonged asbestos exposure

Starts in upper lobes then moves down

Often men >60yo

63
Q

Which asbestos related pleural disease requires the most prolonged asbestos exposure?

A

Asbestosis

64
Q

How do you differentiate between asbestosis and IPF?

Both often men over age 60

A

Asbestosis

  • Decades of working with asbestos (must have long exposure)
  • Similar age of fibrosis on CT
  • Upper lobe predominant

IPF

  • Temporal heterogeneity on CT (pathognomic) - varying ages of fibrosis i.e. some areas with lots of architectural distortion and other areas with little architecture distortion
  • Lower lobe predominant
  • They could have plaques from working with asbestos
65
Q

Mesothelioma

How do they present?

A

Pleural effusion
Chest wall pain (not pleuritic; dull ache that keeps them up at night) - this is due to neural invasion of this tumour into nerve endings into pleura and chest wall

If they have previous asbestos exposure, they have mesothelioma until proven otherwise

66
Q

Mesothelioma diagnosis

A
  • CXR: one big lung, one small lung late stage
  • CT: irregular edges around mediastinum and around lung

Pleural tap will NOT diagnose mesothelioma (all you get is atypical mesothelioma cells which can happen in parapneumonic effusion)

To make the diagnosis, its VATS biopsy. Usually do pleurodesis at the same time.

67
Q

Mesothelioma requires how much asbestos exposure?

A

Usually long exposure

But can be short exposure too - 1-2 days is enough

68
Q

Mesothelioma treatment

A 
Immunotherapy
Pemetrexed (chemo) - prolong survival by a few months only

Average life expectancy is 12 months. Will just wrap around every thing mediastinum, oesophagus.

Not curable

69
Q

Do you try eradicate pseudomonas in bronchiectasis?

A

No
They always have inflammation and sputum in their airways so can’t be eradicated. But can reduce the colony forming units in exacerbations.

Different to other lung disease.

70
Q

How do you treat exacerbation of bronchiectasis (pseudomonas)?

A

2 weeks
2 agents

PO ciprofloxacin + nebulised aminoglycosides

71
Q

What is ABPA?

A

Need either asthma or bronchiectasis to start with

Breathes in aspergillus fiber –> allergic to it (profound IgE response in airway)

72
Q

ABPA diagnostic criteria

A

Asthma or bronchiectasis
Raised IgE
Positive aspergillus precipiant (blood test)
Aspergillus on sputum culture or bronchoscopy

Proximal upper lobe bronchiectasis (chronic)

73
Q

ABPA classic scenarios

A

Classic presentations
1) Asthmatic who normally has a dry cough, starts coughing up sputum plugs

2) Bronchiectasis patient who normally coughs up sputum, but suddenly develops wheeze

74
Q

ABPA treatment

A

Prednisolone (IgE mediated disease) - course duration varies 3/12+

Itraconazole can shorten duration of exacerbation

Can recur
>1 episode: lifelong itraconazole

75
Q

CF bronchiectasis has higher prevalence of aspergillus

True of false

A

True

76
Q 
Common peroneal nerve palsy
Asthma
Eosinophilia 
Cardiac myopathy
Dx
A

EGPA

77
Q

EGPA management

A

Pulse methylpred 3/7
+ immunosuppressant (depending on organ involvement)
E.g CYC for cardiac involvement

ANCA neg more likely to have cardiac disease and more severe

78
Q

Can asbestos related pleural disease look like mesothelioma?

A

Yes
Meso wraps around mediastinum thats quite distinct

Thats why you need a biopsy (VATS)

Don’t get chest wall pain in asbestos related pleural disease

79
Q

What’s SMART protocol in asthma?

A

LABA in symbicort has onset of action 2 min

Has been shown to reduce oral corticosteroid in 12 month period

BUT need good health literacy

80
Q

Most common lung cancer related to smoking

A

Squamous cell carcinoma

81
Q

Biologics in asthma

Do they cause cancer or immunosuppression?

A

Don’t cause cancer or immunosuppression

Very specific anti-IgE, IL5, eosinophilic agents

Theres 15 year data on mepolizumab

82
Q

Is IPF inflammatory?

A

No
Its all fibrotic
Won’t have ground glass changes unlike interstitial pneumonitis, organised pneumonia

83
Q

Problems with putting a chest drain into mesothelioma pleural effusion

A

Cancer may seed through the drain

Consider giving radiotherapy to that site to prevent seeding

84
Q

Exercise induced asthma management

A

Still need low dose asthma

85
Q

Thunderstorm asthma

A

Occurs in Spring
Allergic to rye grass
Before the rain
Rye grass pollenating –> winds before the storm that sweeps the pollen into the clouds –> Lightening/electricity opens up the pollen spores –> breath in spores –> bronchospasm

Mostly relates to people who don’t know they have asthma and just have hayfever

Turn off airconditioners
Close windows
Turn the vents inwards inside cars

Respiratory (7 decks)

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