Brainscape's Knowledge GenomeTM

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


See full index

Medicine > Respiratory > Flashcards

Respiratory Flashcards

bronchiectasis, COPD, lung cancer

1
Q

what is the pathology of bronchiectasis?

A

chronic inflammation of the bronchi + bronchioles leads to permanent dilatation + thinning (elastin fibres) of these airways.

defective muco-ciliary clearance -> infection -> organism persists and inhibits ciliary function further -> colonisation with chronic inflammatory response -> tissue damage -> progressive lung damage

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

what are the main organisms causing bronchiectasis?

A

h influenzae
strep pneumoniae
staph aureus
pseudomonas aeruginosa

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

what are the congenital causes of bronchiectasis?

A

cystic fibrosis
young’s syndrome (bronchiectasis, rhinosinusitis + reduced fertility)
primary ciliary dyskinesia/kartagener’s syndrome

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

what are the post-infection causes of bronchiectasis?

A 
measles
pertussis 
bronchiolitis
pneumonia
TB
HIV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the other causes of bronchiectasis (not infection or post-infection)?

A

bronchial obstruction (tumour, foreign body)
allergic bronchopulmonary aspergillosis (ABPA)
hypogammaglobulinaemia
rheumatoid arthritis
UC
idiopathic

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

what are the symptoms of bronchiectasis?

A

persistent cough
copious purulent sputum
intermittent haemoptysis

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

what are the signs of bronchiectasis?

A

finger clubbing
coarse inspiratory crepitations
wheeze (asthma, COPD, ABPA)

conjunctival pallor- anaemia of chronic disease
pitting oedema
raised JVP/RV heave
thin skin from chronic disease +/- malabsorption
cyanosis

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

what are the complications of bronchiectasis?

A 
pneumonia
pleural effusion 
pneumothorax
haemoptysis 
cerebral abscess
amyloidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what bedside/blood tests would you do for bronchiectasis?

A

serum immunoglobulins
sputum culture
CF sweat test
aspergillus precipitins or skin-prick test RAST and total IgE
spiromotery- obstructive pattern, assess reversibility

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

what imaging and other tests would you do for bronchiecatsis (+ why) ?

A

1- CXR
2- HRCT chest - to assess extent +distribution
3- bronchosopy - locate site of haemoptysis, exclude obstruction and obtain culture samples

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

what would you see on CXR for bronchiectasis?

A

cystic shadows

thickened bronchial walls (tramline and ring shadows)

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

how would you manage bronchiectasis?

A

1- airway clearance techniques + mucolytics - chest physiotherapy + flutter valve aids sputum expectoration + mucus drainage

2- antibiotics- according to bacterial sensitivities

3- bronchodilators eg nebulised salbutamol if asthma, COPD, CF, ABPA

4- corticosteroids eg prednisolone + also itraconazole for ABPA

5- surgery for localised disease or control severe haemoptysis

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

what antibiotics would you give for bronchiectasis if patient is known to culture pseudomonas?

A

oral ciprofloxacin or other IV antibiotics

3 or more exacerbations/year give long-term antibiotics (neublised)

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

what are the general categories for causes of bronchiectasis?

A

localised

  • after severe pneumonia
  • distal to endobronchial obstruction- foreign body, tumour
  • distal to extrabronchial obstruction- tuberculous hilar nodes (Brock’s syndrome)

generalised- immune complexes + persistent infections cause bronchial wall damage

persistent infx- cystic fibrosis, ciliary dyskinesia/kargagener’s sydnrome, mucus abnomrality/young’s syndrome, immune defects (immunoglobulin or complement deficiency, chornc granulomatous disease)

immune complexes- ABPA, RA, IBD.

rare- yellow nail syndrome, A1-antitrypsin deficiency, marfan’s

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

what is COPD?

A

COPD is a progressive disorder characterised by airway obstruction with little or no reversibility

it includes chronic bronchitis + emphysema

FEV1 <80% predicted
FEV1/FVC <0.7

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

what is chronic bronchitis?

A

defined clinically as a cough, sputum production on most days for 3 months of 2 successive years

smoking causes bronchial mucus gland hypertrophy + increased mucus production. early changes in small airways.

symptoms improve if they stop smoking
no excess mortality if lung function is normal

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

what is emphysema

A

defined histologically as enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls

often visualised on CT
destruction of lung tissue with dilatation of distal airspaces, leads to loss of elastic recoil, hyperinflation, gas trapping + increased work of breathing. as the disease progresses, CO2 levels rise and resp drive swtiches from co2 to hypoxaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what would be the differences seen between asthma and COPD?

A

Copd usually age of onset >35yo

passive/active smoking or pollution related
chronic dyspnoea
sputum production
minimal diurnal or day to day FEV1 variation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the symptoms of COPD?

A

cough
sputum
dyspnoea
wheeze

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the signs of COPD?

A

plethoric (high hb)
tachypnoea, bounding pulse
raised systolic (smoking, atherosclerosis)
lowered diastolic (CO2 retention-> vasodilation)
cor pulmonale signs- raised JVP, oedema

agitated (low pO2)
sleepy (high PCO2)
warm hands, metabolic flap (sharp twitch every 5-10s)

use of accessory muscles
hyperinflation- barrel chest
decreased cricosternal distance <3cm
decreased expansion
resonant/hyperresonant percussion note
quiet breath sounds eg over bullae 
wheeze (decreased air entry) 
cyanosis
21
Q

what are the complications of COPD?

A 
acute exacerbations +/- infection
polycythaemia
respiratory failure
cor pulmonale- oedema, JVP
pneumothorax (ruptured bullae)
lung carcinoma
22
Q

what investigations would you want for COPD?

A 
FBC
pulmonary fx tests 
CXR
CT
ECG
ABG if concerned about resp failure 
spirometry
23
Q

what are the results of investigaitons for COPD?

A

FBC- raised pCV
ECG- right atrial + ventriuclar hypertrophy (cor pulmonale)
ABG- decreased PO2 +/- hypercapnia (type 2)

spirometry- obstructive + air trapping (at least 6 seconds)
raised TLC, RV, lowered DLCO in emphysema

24
Q

what results would you expect for CXR for COPD?

A

hyperinflation
flat hemidiaphragms
large central pulmonary arteries less peripheral vascular markings
bullae

25
Q

what results would you expect for CT for COPD?

A

bronchial wall thickening
scarring
air space enlargement

26
Q

what is the first step of COPD management?

A

initiate short acting B2 antagonist SABA eg salbutamol

OR short-acting muscarinic antagonist SAMA eg ipratroprium bromide

27
Q

what is the 2nd step of COPD management after SABA/SAMA if FEV1>50%?

A

long-acting B2 antagonist LABA eg salmeterol

long-acting muscarinic antagonist LAMA eg triotroprium

28
Q

what is the 3rd + 4th step of COPD management after SABA/SAMA and LABA/LAMA if FEV1>50%?

A

LABA plus inhaled corticosteroid

LAMA plus LABA/ICS combination inhaler

29
Q

what is the 2nd step of COPD management after SABA/SAMA if FEV1<50%?

A

long-acting muscarinic antagonist LAMA eg triotroprium

LABA plus inhaled corticosteroid in combined inhaler

30
Q

what is the 3rd step of COPD management after SABA/SAMA and LAMA and LABA/ICS inhaled if FEV1 <50%?

A

LAMA plus LABA/ICS combination inhaler

31
Q

what are the indications for specialist referral for COPD?

A

uncertain diagnosis or suspected severe COPD or rapid decline in FEV1

onset of cor pulmonale
bullous lung disease- assess for surgery

assessment for oral corticosteroids, nebuliser therapy or LTOT

<10pack years or <40yo- alpha1-antitrypsin deficiency

symptoms disproportionate to lung funciton tests

frequent infections - exclude bronchiectasis

32
Q

what is the conservative/other medical management for COPD?

A 
smoking cessation advice 
encourage exercise
diet advice +/- supplements 
mucolytics- chronic prod. cough
flu + pneumococcal vaccinations 
oedema- diuretics
pulmonary rehabilitation

depression- screen for disabilities that can cause this

air travel risky if FEV1<50% or po2<6.7kpa OA

33
Q

what are the indications for LTOT?

A

1- clinically stable non-smokers with pO2 <7.3kpa despite maximal treatment. values should be stable on 2 occasions >3 weeks apart

2- if po2 7.3-8kpa + pulmonary HTN eg RVH, loud S or polycythaemia or peripheral oedema or nocturnal hypoxia

3- terminally ill patients

34
Q

what is the severity assessement in COPD?

A 
BODE index 
body mass indiex
airflow obstruciton
dyspnoea 
exercise capacity

predicts outcome + number + severity of COPD into 4 stages- mild, moderate, severe, very severe based on post-bronchodilator FEV1 predicted

35
Q

when can surgery be considered in COPD patients?

A

recurrent pneumothraces
isolated bullous disease
lung volume reduction/endobronchial valve/transplant

36
Q

what are pink puffers in COPD?

A

raised alveolar ventilation
near normal pO2 + normal/lowPCO2
breathless but not cyanosed
may progress to type 1 resp failure

thinner ones, breathless, emphysema

37
Q

what are blue bloaters in COPD?

A 
low alveolar ventilation
low PO2 + high PCO2
cyanosed but not breathless 
may develop cor pulmonale 
their respiratory centres are insenstiive to CO2 and they rely on hypoxic drive to maintain rest effort so supplementary o2 should be given with care

bigger ones, cyanosis, chronic bronchitis

(look at images online pink puffers/blue bloaters)

38
Q

what is defined as mild COPD?

A

FEV1 80%+ of age/sex predicted

cough, minimal dyspnoea, normal exam

39
Q

what is defined as moderate COPD?

A

FEV1 50-79%

cough, breathless on moderate exertion

wheeze, hyperinflation, reduced air entry

40
Q

what is defined as severe COPD?

A

FEV1 30-49%

cough, breathless on minimal exertion

same as moderate- wheeze, hyperinflation, reduced air entry

and possibly cor pulmonale signs (RHF)

41
Q

what is defined as very severe COPD?

A

FEV1<30% or <50% with resp failure

42
Q

what is the surgical management for COPD?

A

resection of large bullae so adjacent areas of lung reinflate

lung volume reduction surgery can improve elastic recoil and maintain airway patency

lung transplant rare

43
Q

what are the 4 main cellular types of lung cancer?

A

squamous
adenocarcinoma
small scale
large cell

44
Q

what are the features of squamous lung cancer?

A

large airways affected
slow growth
late metastases
cavitation occurs

45
Q

what are the features of adenocarcinoma lung cancer?

A 
peripheral lung 
non-smokers more common
slow growth 
metastases earlier than squamous 
alveolar cell subtype grows slowly and spreads via airways

associated with mutations of EGFR which can affect response to chemo
epidermal growth factor receptor

46
Q

what are the features of small cell carcinoma lung cancer?

A

central
rapid growth
early metastases- often presents with extensive disease

47
Q

what are the features of large cell lung cancer?

A

intermediate type- progression/spread between that of squamous and small cell

in terms of metastases- small cell fast, then adeno/large cell, squamous slowest

48
Q

what is the aetiology.causes of lung cancer?

A

tobacco- 85% of lung cancers (not adenocarcinoma)

passive smoking
occupational exposure to asbestos, silica, nickel
pulmonary fibrosis
genetic factors

Medicine (3 decks)

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