Resp Flashcards

1
Q

cardinal symptoms for respiratory system?

A
dyspnoea
chest pain
cough
hamoptysis
sputum production
wheeze
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2
Q

what is sarcoidosis and what are some of its symptoms/signs?

A
multisystem granulomatous disorder
dry cough
progressive dypnoea
chest pain
reduced exercise tolerance
lymphadenopathy
hepatomegaly
splenomegaly
renal stones
erythema nodosum
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3
Q

resp causes of clubbing?

A
lung cancer
cystic fibrosis
COPD?
TB
interstitial lung disease- fibrosing alveolitis
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4
Q

sound hear on auscultation in a patient with a pleural rub e.g. due to pleuritis, pneumonia spread, (and pericardial rub e.g. pericarditis)

A

like footprints on fresh snow, or rusting leaves

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5
Q

sound heard on auscultation in a patient with crepitations/crackles e.g. in pneumonia, pulmonary oedema?

A

like rice krispies- popping sound- as narrow airways forced shut during expiration re-open in inspiration

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6
Q

what should you look for when observing a patient’s outstretched hands from the side during a respiratory exam?

A

a tremor- may be due to beta 2 agonist e.g. salbutamol used in asthma. Short-acting beta 2 agonist= 1st line, 3rd= long acting beta 2 agonist e.g. salmeterol or formoterol.
(ADRs = tachycardia, skeletal muscle tremor, palpitations)

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7
Q

what gives a dull percussion note?

A

pleural effusion- stony dull
consolidation e.g. pneumonia
fibrosis
pleural thickeing

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8
Q

what gives a hyperesonant percussion note?

A

pneumothorax

lung hyperinflation e.g. COPD

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9
Q

what gives diminished breath sounds on auscultation?

A
pleural effusion
pneumothorax
asthma
COPD
pleural thickeing
bronchial obstruction
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10
Q

what may produce increased vocal resonance on auscultation?

A

consolidation e.g. pneumonia

above a pleural effusion

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11
Q

in what conditions might a wheeze be heard?

A

tumour obstructing 1 airway- monophonic

asthma- polyphonic and widespread airflow obstruction

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12
Q

what is a wheeze?

A

a high pitched expiratory sound, like a whistle
occurs due to vibration of intra-thoracic airway wall in at site of airflow limitation. More pronounced in expiration as airways narrower than in inspiration due to compression of small airways to force air out of the lungs, worsening the narrowing.

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13
Q

what is stridor?

A

inspiratory sound due to partial obstruction of upper airways.
Maybe due to something within lumen e.g. oedema from anaphylaxis, laryngospasm, tumour
or extrinsic e.g. goitre, oesophagus, lymphadenopathy

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14
Q

why is apex beat felt for on resp examination?

A

if impalpable, may indicate COPD, pleural effusion

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15
Q

differentials for bilateral basal crackles?

A

pulmonary oedema
interstitial lung disease
bronchiectasis

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16
Q

why does TB tend to affect upper lobes of lung?

A

more air, better O2 supply

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17
Q

causes of clear and colourless sputum?

A

COPD- chronic bronchitis

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18
Q

causes of yellow-green sputum?

A

pulmonary infection- pneumonia, TB

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19
Q

causes of red sputum?

A

haemoptysis- TB, lung cancer, PE, GoodPasture’s syndrome

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20
Q

cause of pink and frothy sputum?

A

pulmonary oedema in L sided heart failure

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21
Q

cause of black sputum?

A

smoke

coal dust

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22
Q

what happens to sputum when sent off to laboratory?

A

microscopy- gram staining
culture
cytology

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23
Q

how is peak expiratory flow measured?

A

maximal forced expiration through a peak flow meter

more effort-dependent than FEV1.0

24
Q

factors affecting peak expiratory flow?

A

age
gender
height

25
Q

range of peak expiratory flow expected for women?

A

400-500 L/min for women aged between 15 and 65

26
Q

range of peak expiratory flow expected for men?

A

520-660 L/min for men aged between 15 and 55

27
Q

what can cause incorrect readings with pulse oximetry?

A
poor perfusion
motion
excess light
skin pigmentation
nail varnish
dyshaemoglobinaemias e.g. thalassaemia
CO poisoning
28
Q

what does pulse oximetry measure?

A

non-invasive assessment of peripheral O2 saturation

and HR

29
Q

difference between vesicular breath sounds and bronchial breathing?

A
vesicular= rustling quality
bronchial= heard normally over large airways e.g. trachea, hollow quality, can occur where lung tissue has become firm e.g. pneumonia consolidation, or fibrosis
30
Q

characteristic of chest pain resulting from a respiratory cause?

A

pleuritic= worse on inspiration

31
Q

what do I want once completed respiratory examination

A

examine any sputum
perform peak flow
temperature

32
Q

what chest deformities may be visible in respiratory disease?

A

barrel chest- AP diameter increased, tracheal descent, reduced chest expansion, seen in chronic hyperinflation e.g. COPD, asthma
pigeon chest- pectus carinatum- lung hyperinflation whilst bony thorax still devloping e.g. in chronic childhood asthma
funnel chest- pectus excavatum- assoc with Marfan’s syndrome and scoliosis, developmental defect involving local sternum depression.
kyphosis- increase AP thoracic spine curvature
scoliosis- lateral curvature
ALL can cause restrictive lung defect- FEV1.0/FVC ratio >70%

33
Q

what may cause trachea/mediastinal shift towards pathology?**

A

lobe collapse/spontaneous pneumothorax

fibrosis

34
Q

what may cause trachea/mediastinal shift away from pathology?

A

pleural effusion

tension pneumothorax

35
Q

what do you want to ask a patient specifically about if thinking asthma?

A

precipitants= cold air, exercise, smoking, allergens e.g. fur from pets at home, emotion
diurnal variation in symptoms- cough worse at night? stopping them from sleeping, nights per wk?, performance at school reduced? dyspnoea on a morning?
dyspnoea- what does it stop you from doing? exercise tolerance?
acid reflux?
PMH: other atopic disease e.g. eczema, hayfever
FH: atopic disease?
SH: home- pets? carpet?
nonsmoker?- unlikely to be COPD
job e.g. paint sprayer, animal handler

36
Q

how can asthma and COPD be distinguished between with spirometry?

A

> /15% in FEV1.0 with bronchodilators (beta 2 agonists) in asthma as reversible, <15% improvement in COPD as irreversible.

37
Q

Differential diagnoses for asthma?

A

COPD- irreversible- spirometry, almost all patients smokers or have smoked in past, symptoms all the time as chronic, not related to precipitating factors and time of day, tend to be older patients.
large airway obstruction e.g. foreign body, tumour
pulmonary oedema
malginancy
SVC obstruction- but wheeze/dyspnoea not episodic
pneumothorax
PE
bronchiectasis
interstitial lung disease- dry cough
pulmonary fibrosis
gastro-oesophageal reflux- nocturnal cough
in children consider bronchiolitis, cystic fibrosis- persistent cough and infections, foreign body obstructing large airway, recurrent childhood infections.

38
Q

typical symptoms of asthma?

A

dry cough- worse at night
dyspnoea- worse on a morning
wheeze
chest tightness

39
Q

describe what asthma is to a patient, and how it comes about

A

from time to time, the small airways known as bronchi, which carry air to and from the lungs, become narrowed producing the symptoms experienced. These airways are more sensitive than normal to certain things such as cold air and pet fur. Normally, air taken in through large airway= trachea, down into lungs via smaller airways, and then oxygen from air can pass into you blood by crossing small air sacs in the lungs, and so can get to all the different parts of the body requiring oxygen.
Inflammation of the bronchi occurs and when you come into contact with something that irritates your lungs – known as a trigger – your airways become narrow, the muscles around them tighten, and there is an increase in the production of sticky mucus (phlegm), which makes air entry into the lungs more difficult, so you may feel breathless.
Mucus production may cause you to cough, but dry cough?* as mucous plugging?- body trying to get rid of it but can’t? and limit airflow, so breathless.
wheeze- due to restriction of air flow to and from lungs.
The cause isn’t known, but people are more likely to get asthma if others in their family have it, or other atopic conditions e.g. eczema and hayfever- body more sensitive than other people’s to substances e.g. pollen.

40
Q

how is asthma investigated?

A

spirometry

peak flow

41
Q

tment of asthma?

A

reliever and preventor medication- must take preventor even if not experiencing symptoms to protect airways from being damaged?*

42
Q

key management aim in COPD patient?

A

smoking cessation
want to reduce risk of exacerbations and admission to hospital, improve QOL and ability to cope with symptoms e.g. dyspnoea- try and improve exercise tolerance e.g via pulmonary rehabilitation- 6wk programme.

43
Q

how is it important to quantify dyspnoea/pain?

A

what does it stop you from doing? is your ability to do daily activities affected? how does this make you feel (consider psychosocial aspect)?

44
Q

pharmacologic management of asthma?

A

short acting beta 2 agonist e.g. salbutamol, terbutaline
inhaled corticosteroid e.g. beclometasone
long acting beta 2 agonist e.g. salmeterol, may be in combination inhaler with inhaled corticosteroid e.g. symbicort= formoterol and budesonide?
add on therapies= xanthines, muscarinic antagonists e.g. tiotropium bromide, LRAs
oral corticosteroid- prednisolone

also want to tell patients to avoid triggers, comply with therapy, educate them and parents about symptoms of acute attacks.

45
Q

main symptoms of COPD?

A

progressive disease, cough with clear and colourless sputum- as damaged airways make more mucus than normal
exertional dyspnoea- can’t get enough air into lungs through obstructed airways, progressively worsens
possibly wheeze- obstructed airways, walls vibrate, aways compressed in expiration- worsens narrowing

46
Q

what is copd, explain to patient

A

term to describe 2 conditions: chronic bronchitis and emphysema. persistent condition, will have for life but management, especially smoking cessation, will control symptoms, and stopping smoking can improve function of airways.
chronic bronchitis= inflammation of bronchi= lung airways
emphysema= damage to smaller airways and air sacs (alveoli) in lung which allow O2 from air to get into our blood. COPD= persistent, air flow obstructed to and from lungs, affecting lungs.
cause= usually smoking= smoke irritates airways, causes damage, promoting inflammatory response. degree of genetic risk- lack an important protein for keeping appropriate structure of smaller airways and air sac for air movement.

at risk of chest infections- mucus build up good for bacteria, can worsen symptoms= exacerbation, so report to dr and can treat with antibiotics.
also of heart failure= heart unable to work as well so can’t pump blood around body as effectively as normal as lung tissue damage with COPD puts an increased strain on the heart as heart has to pump blood through the damaged lungs- breathlessness may worsen and may find swelling of ankles. Treatment= ACEIs and beta blockers, possibly aldosterone antagonsit diuretic.
and resp failure

47
Q

tments for COPD?

A

STOP SMOKING- can’t reverse airway narrowing but prevents disease worsening, stops airway function from decreasing as fast as it would with smoking, reduces symptoms.
No treatment is CURATIVE.
inhalers= short acting bronchodilators to relax smooth muscle of airways to open them up, long-acting if symptoms remain problematic.
steroid inhaler- reduce inflammation, can help prevent symptoms flaring up. Only used with long term bronchodilator. And may increase dose of usual tments.
mucolytics= make sputum less thick and easier to cough up, must take regularly, can help reduce flare ups as less risk of infection as less mucus for bacteria.
may give steroid tablets e.g. prednisolone, and antibiotics for flare ups.
home O2 if severe
regular exercise
lose weight

48
Q

differentials for COPD?

A

asthma- trigger factors, diurnal variation, history of atopy, non smoker
bronchiectasis- LOTS of sputum, intermittent hamoptysis
TB- night sweats, hamoptysis, FH, contacts, weight loss
malignancy- weight loss, fatigue, chest pain
intersitial lung disease
congestive heart failure- with pulmonary oedema- dyspnoea wakes you up, have to sleep with more pillows to stop feeling breathless? ankle swelling? raised JVP?
anaemia

49
Q

4 differentials for sudden onset chest pain?

A

trauma
MI
pneumothorax
aortic dissection- causes radial-radial delay

50
Q

pathology in PE which causes type 1 respiratory failure?

A

ventilation/perfusion mismatch- as embolus obstructs flow of blood, blood is away, which means that actually too much blood is reaching alveoli for the ventilation available, and it is this which causes the problem= hypoxia= pO2<8.0 kPa.

51
Q

what might you seen on inspection of a patient with a pneumothorax?

A

reduced chest expansion on affected side
trachea deviation away from affected side (if tension pneumothorax- these are more common and more dangerous as air can only travel 1 way in pleural sac, so air accumulates*) trachea deviated towards affected side in spontaneous pneumothorax.

52
Q

what might you hear on auscultation of a patient with a pneumothorax?

A

diminshed/absent breath sounds on affected side

53
Q

characteristic signs of patient with interstitial lung disease?

A

bilateral fine inspiratory crackles/crepitations

clubbing

54
Q

signs in a severe acute asthmatic attack?

A

pulse >110bpm
RR>25 breaths/min
PEFR between 33 and 50% of that predicted or best
unable to complete sentences

55
Q

signs in life threatening asthma attack?

A

paCo2 increasing/high, PEFR<33% of that predicted or best

56
Q

Tment of severe acute asthmatic attack?

A

high dose O2
nebulised salbutamol and ipratropium bromide with O2
oral prednisolone or IV hydrocortisone

do CXR to exclude pneumothorax

57
Q

what may cause reduced vocal resonance on auscultation?

A

pleural effusion