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Resp Flashcards

1
Q

What can cause upper zone lung fibrosis

A 
TB
extrinsic allergic alveolitis
sarcoidosis
silicosis
ank spond
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2
Q

What can cause lower zone lung fibrosis

A

IPF
drugs
asbestosis

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3
Q

What drugs can cause lower zone lung fibrosis

A

amiodarone
methotrexate
bleomycin
nitrofurantoin

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4
Q

What is idiopathic pulmonary fibrosis

A

progressive fibrosis of the interstitial alveolar tissue
excessive collagen deposition
no known cause

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5
Q

Who is IPF most common in

A

men aged 50-70

smokers

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6
Q

What are the symptoms of IPF

A

dry cough

SOB

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7
Q

What are the signs of IPF

A

fine end-inspiratory bibasal crackles

clubbing

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8
Q

How should a patient with suspected IPF be investigated?

A 
Bedside
Bloods: ABG, ANA, CRP
Micro: 
Imaging: CXR, HRCT, 
Special tests: spirometry, TLCO
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9
Q

What are the common findings on CXR in IPF

A

reticular shadowing
small, irregular, peripheral opacities - ground-glass
decreased lung volume
honeycombing

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10
Q

What are the common findings on HRCT in IPF

A

reticular opacities
honeycombing

essential for diagnosis!

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11
Q

What are the common findings on spirometry in IPF

A

reduced FVC
reduced FEV1
FEV1/FVC normal/increased

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12
Q

What What are the common findings on TLCO in spirometry

A

reduced transfer factor

impaired gas exchange

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13
Q

What is the management of IPF

A

pulmonary rehabilitation
oxygen

clinical trial
lung transplant

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14
Q

What is the prognosis in IPF

A

50% 5 year survival rate

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15
Q

What investigations should be carried out in suspected COPD

A 
Bedside: BMI, ECG
Bloods: FBC, 
Micro
Imaging: CXR
Special tests: post bronchodilator spirometry
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16
Q

State the MRC Dyspnoea Scale grades

A 
1 = not breathless
2 = breathless on walking up hill
3 = walks slowly
4 = breathless after 100 metres/ few mins
5 = unable to leave house
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17
Q

How are the stages of COPD defines

A

perventage predicted of FEV1

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18
Q

State the stages of COPD defined by the FEV1

A 
>80% = mild
50-79% = moderate
30-49% = severe
<30% = very severe
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19
Q

What are the signs of COPD on CXR

A

increased lung volume
flattened diaphragm
bullae

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20
Q

Describe the steps in the pharmacological management of stable COPD

A
  1. LABA/LAMA
  2. if FEV1 >50% = LABA/LAMA
    if FEV1 <50% = LABA+ICS/LAMA
  3. if LABA -> LABA+ICS
    if LAMA -> LABA+ICS + LAMA
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21
Q

What general measures are involved in the management of COPD

A

pulmonary rehabilitation
stop smoking
influenza vaccine
pneumococcal vaccine

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22
Q

What bacteria are most commonly present in acute exacerbation of COPD

A

Haemophilus influenzae
Streptococcus pneumoniae
Moraxella catarrhalis

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23
Q

Descrebe the steps in management of an acute exacerbation of COPD

A 
admit
nebulised salbutamol and ipatropium
oxygen - if known hypercapnic, 28% venturi(white) at 4l
IV hydrocortisone and oral presnisolone
Abx if sputum purulent - doxycycline
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24
Q

What is the rationale behind LTOT in COPD

A

maintaining PaO2 >8kPa for >15hours per day increases the 3yr survival rate by 50%

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25
Q

What are the criteria for LTOT in COPD

A

PaO2 <7.3 on two separate occasions greater then 3 weeks apart

PaO2 7.3-8 + evidence of pulmonary hypertension, polycythaemia, peripheral oedema, nocturnal hypoxia on two separate occasions greater then 3 weeks apart

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26
Q

Which patients with COPD should be assessed for LTOT

A

very severe airflow obstruction (FEV1 < 30% predicted), ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
cyanosis
polycythaemia
peripheral oedema
raised JVP
oxygen saturations less than or equal to 92% on room air

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27
Q

What are the diagnostic criteria should be used when assessing a patient with suspected COPD?

A

FEV1/FVC <70%

symptoms!

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28
Q

What is the difference between a primary and secondary pneumothrax?

A 
primary = no underlying disease
secondary = occurs in presence of underlying disease`
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29
Q

What is the difference between a pneumothorax and a tension pneumothorax?

A

tension = trachea deviated away from affected side.

Air cannot leave pleural cavity during expirations due to valve like flap in parietal pleura.

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30
Q

What tests should be done in suspected pneumothorax?

A

ABG

CXR

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31
Q

What is the management of a primary pneumothorax?

A

> 2cm or breathless = aspiration.
successful (<2cm)
= discharge, r/v OPD in 2-4wks
unsuccessful = admit, chest drain

<2cm, not breathless
= discharge, OPD in 2-4wks

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32
Q

What is the management of a secondary pneumothorax?

A

> 2cm, breathless
= chest drain

1-2cm
= aspirate.
success (<1cm) = admit, oxygen, observe 24h
unsuccessful = chest drain

<1cm = admit, oxygen, observe 24h

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33
Q

How do you aspirate a pneumothorax

A

14-16G cannula
2nd ICS in midclavicular line (superior to 3rd rib)
remove needle
connect cannula to 3 way tap and 50ml syringe
aspirate!
CXR to confirm resolution

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34
Q

What are the signs of a working chest drain?

A

swinging
bubbling
water bottle below patient!

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35
Q

What is the bacterium involved in TB

A

Mycobacterium tuberculosis

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36
Q

What are the characteristics of the Mycobacterium tuberculosis

A

aerobe
rod shaped
waxy - acid fast

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37
Q

Describe how the ghon focus forms in TB

A 
Macrophages phagocytose bacteria
Tb can inhibit phagosome and lysosome fusing
TB proliferates
granuloma forms
caseous necrosis
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38
Q

What are the cells in a granuloma

A

epitheloid histiocytes

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39
Q

What is a Ghon complex

A

ghon focus plus hilar lymph node involvement

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40
Q

What is a Ranke complex

A

fibrosis and calcification of Ghon complex

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41
Q

What can cause dormant TB to become reactivated

A 
steroids
HIV
malnutrition
chronic renal failure
solid organ transplantation with immunosuppression
IVDU
haematological malignancy
anti-TNF treatment
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42
Q

Where is TB often located in the lungs?

A

upper lobes

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43
Q

Where can TB spread to?

A 
brain - meningitis
kidneys - sterile pyuria
spine - Pott's
adrenal - addison's
liver - hepatitis
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44
Q

What investigations should be done in suspected TB

A

sputum cultures - 3x

CXR

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45
Q

What are the features of TB on CXR

A 
hilar lymphadenopathy
consolidation in upper lobes
Ghon focus
upper zone fibrosis
pleural effusion in primary
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46
Q

What is the treatment for active TB

A

Rifampicin
Isoniazid
Pyramidazole
Ethambutol

R+I for 6m, P+E for first 2 months

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47
Q

What is the treatment for latent TB

A

Rifampicin and Isoniazid for 3m

Isoniazid for 6m

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48
Q

What are the side effects of rifampicin

A

hepatitis, orange secretions

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49
Q

What are the side effects of isoniazid

A

peripheral neuropathy
hepatitis,
agranulocytosis

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50
Q

What are the side effects of pyrazinamide

A

hyperuricaemia causing gout
arthralgia,
myalgia
hepatitis

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51
Q

What are the side effects of ethambutol

A

optic neuritis

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52
Q

What tests do you need to do before initiating treatment of TB

A

LFTs
visual acuity
FBC

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53
Q

What is the difference between acute bronchitis and pneumonia?

A

acute bronchitis is a transient inflammation of the trachea and major bronchi associated with oedema and mucus production

pneumonia is an acute infection of the lung parenchyma

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54
Q

State the most common causes of CAP

A

Streptococcus pneumoniae
Haemophilus influenzae
Staphylococcus aureus

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55
Q

What are some atypical causes of CAP

A

Mycoplasma pneumoniae
Klebsiella pneumoniae
Legionella pneumophilia
Pneumocystis jiroveci

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56
Q

What are the common features of pneumonia causes by Streptococcus pneumoniae

A

fever
rapid onset
pleuritic chest pain
cold sores!

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57
Q

Which group of people is Klebsiella pneumoniae most common in?

A

alcoholics

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58
Q

Which bacterial cause of pneumonia often follows influenza?

A

staph aureus

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59
Q

What chsnegs are often seen in teh blood results of a patient with Legionella pneumophilia?

A

lymphopaenia
hyponatraemia
deranged LFTs

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60
Q

What are the classical features of Pneumocystis jiroveci

A

HIV positive
dry cough
no chest signs
desaturate on exercise

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61
Q

What are the most common causes of HAP

A

gram negative enterobacteria
staph aureus
Moraxella catarrhalis

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62
Q

What are the most common causes of pneumonia in an immunocompromised patient?

A 
Strep pneumoniae
Haemophilus influenzae
Staph aureus
Moraxella catarrhalis		
Mycoplasma pneumoniae 	
Pneumocystis jiroveci
CMV			
HSV
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63
Q

What investigations are carried out in suspected pneumonia?

A

urine testing for pneumococcal antigen
FBC, U+E, LFTs, CRP
blood cultures, sputum cultures
CXR

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64
Q

What is the immediate management of a patient with penumonia

A

O2 if desaturated
IV fluids if dehydrated
analgesia for pleuritic pain
antibiotics!

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65
Q

What are the values used for CURB-65

A 
Confusion
Urea >7
RR >30
BP <90/60
>65
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66
Q

How does management change depending on the CURB-65 score?

A

<=1 manage at home
>=2 admission to hospital
>=3 consider ITU/HDU

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67
Q

What is antibiotic treatment for mild/moderate pneumonia

A

amoxicillin 500mg-1g/8h oral for 5 days

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68
Q

What is antibiotic treatment for severe pneumonia

A

7-10days of co-amoxicav 1.2g/8g IV + clarithromycin 500mg/12h IV

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69
Q

What is antibiotic treatment for hospital acquired pneumonia

A

gentamicin plus ceftriaxone

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70
Q

What is the most common cause of PE

A

DVT

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71
Q

What are the most common signs of PE

A

increased RR
increased HR
crackles on auscultation
pyrexia

72
Q

What investigations should be carried out in suspected PE

A

Well’s score

ECG
FBC, U+E, clotting, ABG
CXR to exclude other diagnoses

73
Q

State how to calculate the PE Well’s score

A

Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative) 1

74
Q

How does the Wells score for PE change the investigation of PE

A

> 4 = PE likely. urgent CTPA needed

<=4 = PE unlikely. do d-dimer.
if negative, d-dimer ruled out
if positive, d-dimer not ruled out. arranged CTPA

75
Q

What is the management of a confirmed PE

A

LMWH - enoxaparin 1.5mg/kg/24h plus warfarin

stop LMWH when INR 2-3 for over 24hrs

warfarin for 3m if provoked, 6m if unprovoked

76
Q

What is the management of a massive PE

A 
SENIOR HELP
oxygen
IV access
morphine and antiemetic
IV colloids
thrombolysis
77
Q

What is a massive PE

A

PE with presence of circulatory failure

78
Q

When would V/Q testing be used in investigation of PE

A

if severe renal failure or allergy to contrast

79
Q

Describe the pathophysiology of asthma

A

chronic inflammation of the airways due to a hypersensitivity reaction.
infiltration of eosinophils, TH2 cells and mast cells into the mucosa
release of histamine, leukotrienes and prostaglandins
leading to bronchoconstriction and increased mucus production
airway hypersensetivity
in the long term, there is mucosal oedema and thickened basement membrane

80
Q

What are soem of the risk factors for asthma

A 
developed country
history of atopy
urban areas
premature
viral infection early in life
81
Q

What are the symptoms of asthma

A

cough - dry, worse at night
chest tightness
breathlessness

82
Q

What are the potential triggers of asthma exacerbation

A

dust, pet hair, pollen
air pollutants, smoking, cold air
aspirin, B blockers
occupation

83
Q

What are the signs of chronic asthma

A 
increased RR
hyperinflated chest
use of accessory muscles
intercostal recession
expiratory high pitched wheeze
84
Q

What investigations should be carried out in suspected chronic asthma

A

peak flow monitoring
spirometry with bronchodilator reversibility test
fractional exhaled nitric oxide

85
Q

What are the expected findings on peak flow monitoring in asthma

A

diurnal variation - morning dipping

86
Q

What are the expected findings on spirometry with bronchodilator reversibility testing in asthma

A

FEV1/FVC <70% pre bronchodilator

improvement of >=12% post bronchodilator

87
Q

What is a fractional exhaled nitric oxide test?

A

measurement of nitric oxide synthases in breath

there are 3 types of nitric oxide synthases (NOS) - One of the types is inducible (iNOS) and levels tend to rise in inflammatory cells, particularly eosinophils.

Levels of NO therefore typically correlate with levels of inflammation.

88
Q

What are the expected findings on fractional exhaled nitric oxide test in asthma

A

raised levels due to inflammation

89
Q

What are the steps in management of chronic asthma according to NICE

A
  1. SABA reliever therapy
    • low dose ICS
    • LTRA
    • LABA
  5. lose dose MART
  6. medium dose MART
  7. high dose ICS or LAMA or theophylline
90
Q

What is a LTRA

A

leukotriene receptor antagonist eg. monteleukast

reduced smooth muscle cell constriction, mucus production and eosinophils

91
Q

What is a MART

A

Maintenance and reliever therapy

= combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required

92
Q

Define a moderate acute asthma attack

A

PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm

93
Q

Define a severe acute asthma attack

A

PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

94
Q

Define a life threatening asthma attack

A

any one of:

PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
95
Q

Define a near fatal asthma attack

A

rise in PaCO2 or requiring ventilation

96
Q

What investigations should be carried out in acute asthma attack

A 
PEFR, ECG, pulse oximetry
ABG
FBC, U+E, CRP, 
cultures
?CXR
97
Q

What is the management of severe acute asthma

A

O2 if sats <92%
salbutamol 5mg nebulised with o2 ervy 15 mins
hydrocortisone 100mg IV
ipatropium bromide if response to beta agonists is poor
Abx if due to infection

magnesium sulphate IV if poor response

98
Q

What monitoring needs to be done with salbutamol therapy in acute asthma

A

ECG - tachyarrythmias
potassium - hypokalaemia
peak flows!
ABGs

99
Q

What are the indications for admission to ITU in severe asthma attack?

A 
rising PaCO2
low PaO2
exhaustion, drowsiness, coma
respiratory arrest
not responding to therapy
100
Q

When would it be right to admit a patient with a moderate acute asthma exacerbation to hospital?

A

if they have had a previous near fatal asthma attack

101
Q

When would you consider stepping up chronic asthma therapy

A

using SABA three times a week or more,
being symptomatic three times a week or more,
experiencing night-time symptoms at least once a week,
has had an asthma attack in the last 2 years.

102
Q

Describe the pathophysiology of bronchiectasis

A

chronic infection and inflammation leads to dilation of the bronchial walls and bronchioles

103
Q

What are some causes of bronchiectasis

A

infections: pneumonia, TB, whooping cough, measles
CF
bronchial obstruction e.g. lung cancer/foreign body
immune deficiency: selective IgA, hypogammaglobulinaemia
allergic bronchopulmonary aspergillosis (ABPA)
ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome

104
Q

What are the symptoms of bronchiectasis

A

cough
sputum
haemoptysis

105
Q

What are the signs of bronchiectasis

A 
clubbing
anaemia
coarse crackles on inspiration
cor pulmonale - raised JVP, peripheral oedema
smelly breath - foetor
106
Q

What investigations need to be carried out for bronchiectasis

A

CXR, HRCT
spirometry with reversibility
bronchoscopy

107
Q

What are the typical findings on CXR for bronchiectasis

A

tram lines

108
Q

What are the typical findings on HRCT for bronchiectasis

A

signet ring sign

109
Q

What is the management of bronchiectasis

A

chest physio - twice daily postural drainage
antibiotics in exacerbation (may need to be long term if severe)
bronchodilators if they help
surgery if localised disease

110
Q

What are some complications of bronchiectasis

A

pleural effusion
pneumothorax
pneumonia
cerebral abscess

111
Q

What are the most common organisms found in the sputum of bronchiectasis

A

Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae

112
Q

Name the types of lung cancer

A

small cell
squamous cell
adenocarcinoma
large cell

113
Q

Which lung cancer is more common in non-smokers

A

adenocarcinoma

114
Q

Which lung cancer is PTHrP released in

A

squamous cell

115
Q

Which lung cancer is ADH released in

A

small cell

116
Q

Which lung cancer is ACTH released in

A

small cell

117
Q

Which lung cancer is clubbing more common in

A

squamous

118
Q

Which lung cancers metastasise early and late

A 
early = small and large
late = squamous and adeno
119
Q

What are the most common symptoms of lung cancer

A 
cough
hamoptysis
dyspnoea
chest pain
weight loss
recurrent pneumonia
120
Q

What are the signs of lung cancer

A

cachexia
clubbing
supraclavicular/axillary lymph nodes

121
Q

What are some potential complications of lung cancer

A 
SVC obstruction
phrenic nerve palsy
recurrent laryngeal nerve palsy
Horner's
oesophagel compression
122
Q

What are the features of SVC obstruction

A

swelling of face and upper limbs

dilated veins

123
Q

What are the features of phrenic nerve palsy

A

raised hemidiaphragm on CXR

dyspnoea

124
Q

What are the features of recurrent laryngeal nerve palsy

A

hoarse voice

aspiration

125
Q

What causes Horner’s syndrome in lung cancer

A

palsy of sympathetic chain from Pancoast tumour in apex of lung

126
Q

What are the features of Horner’s syndrome

A

hemifacial anhidrosis
miosis - small pupil
ptosis

127
Q

What investigations should be carried out in suspected lung cancer

A 
CXR
FBC, U+E, bone profile, ACTH and cortisol levels, LFTs, INR
CXR
staging CT
PET scan to look for metastasis
128
Q

What is the WHO performance status scale

A 
0 = normal activity
1 = symptomatic, but ambulatory
2 = >50% normal activity, some help with care
3 = <50% normal activity, needs nursing care
4 = bed bound
129
Q

What is the treatment, according to stage, of lung cancer

A

I or II = curative surgery
IIIa = curative surgery + adjunct chemo
III or IV + performance status 0-2 = chemo

others palliative

130
Q

What kind of things can be done for palliative care in lung cancer

A

radiotherapy - reduce size of tumour

SVC stent

131
Q

What are the common adverse effects of salbutamol

A 
angiooedema
tremor
palpitations
nausea
headache
taste alteration
risk of hypokalaemia
132
Q

Why might salbutamol be contraindicated?

A

hypokalaemia
hypersensetivity
pre-eclampsia

133
Q

What is the mechanism of action of theophylline

A

xanthine

relaxes smooth muscle - acting mainly as a bronchodilator and vasodilator

134
Q

What can affect the plasma-theophylline concentration

A

plasma-theophylline concentration is increased in:
heart failure,
hepatic impairment
viral infections.

The plasma-theophylline concentration is decreased:
in smokers
by alcohol consumption.

Differences in the half-life of theophylline are important because the toxic dose is close to the therapeutic dose.

135
Q

What problems can theophyline cayse

A

hypokalaemia

overdose can be fatal

136
Q

What is the presentation of theophylline overdose

A 
vomiting (which may be severe and intractable), 
agitation, 
restlessness, 
dilated pupils, 
sinus tachycardia, 
hyperglycaemia. 
More serious effects are 
haematemesis, 
convulsions
supraventricular and ventricular arrhythmias. 
Severe hypokalaemia may develop rapidly.
137
Q

What are the key side effects if glucocorticoids?

A 
diabetes
osteoporosis
avascular necrosis of the femoral head.
infections
Muscle wasting (proximal myopathy) can also occur.
peptic ulceration and perforation.
Psychiatric reactions may also occur.
138
Q

What should you tell a patient when presciribing prednisolone?

A

increased risk of infections - see doctor straighwaay
steroid treatment card
if diabetic, check blood more frequently
some immunisatoins might not be suitable - check!
see doctor if any worrying side effects

139
Q

Describe the pathophysiology of COPD

A

progressive airflow obstruction due to mucous gland hyperplasia and loss of cilial functon

emphysema = alveolar wall destruction causing irreversible enlargement of airspaces distal to teh terminal bronchioles
bronchitis = chronic inflammation and fibrosis of small airways due to lymphocytes and macrophages
140
Q

Why do people with COPD develop ankle oedema

A 
hypoxic vasocontriction in lungs
pulmonary hypertension and venous congestion
increased pressure in right ventricle
increased preload
venous
141
Q

Why might uncontrolled oxygen therapy be dangerous in COPD

A

chronic hypercapnia - compensated for by HCO3-
switch to hypoxic respiratory drive
increased oxygen leads to decreased ventilation
worsens hypercapnia

142
Q

What key questions would you ask a patient asthma when reviewing them

A 
cough
SOB
how often using inhalers
inhaler technique
nocturnal sx
exposure to tobacco smoke
school/work/home interference
asthma attacks
steroids?
do they have self-management plan
143
Q

What should be monitored in those taking long term steroids?

A

Blood pressure.
Urine or blood sugar (measured by HbA1c).
Cholesterol.
Bone mineral density.
Vision (to assess for cataracts and glaucoma).

144
Q

What is Allergic Bronchopulmonary Aspergillosis

A

allergic reaction to Aspergillus fumigatus spores

hypersensitivity reaction I or III

145
Q

What are the features of Allergic Bronchopulmonary Aspergillosis

A

first bronchoconstriction - wheeze, cough, SOB

then bronchiectasis - sputum

146
Q

What are the findings on investigation of Allergic Bronchopulmonary Aspergillosis

A

eosinophilia
rasied serum IgE
aspergillus in sputum
positive radioallergosorbent (RAST) test to Aspergillus
CXR: transient segmental collapse or consolidation, bronchiectasis

147
Q

What is an asthma managemnt plan

A

written plan for helping patients to:
recognise worsen asthma - sx or peak flow

initiate changes to treatment when symptoms change eg. seeking emergency help, starting oral steroids, restarting or temporarily increasing inhaled corticosteroid

know how and when to access medical help

148
Q

What are some systemic complications of CAP

A

sepsis
brain abscess
pericarditis
cholestatic jaundice

149
Q

What are some local complications of CAP

A

pleural effusion
empyema
lung abscess
respiratory failure

150
Q

What is the differential diagnosis for a pleural effusion associated with CAP

A

empyema’

secondary to lung cancer

151
Q

What is a pleural effusion

A

collection of excess fluid in the pleural space

152
Q

What is the pathophysiology of a transudate pleural effusion

A

increased hydrostatic or decreased oncotic pressure leading to too much fluid leaving capillaries and entering pleural space

153
Q

What are some causes of a transudate pleural effusion

A

heart failure
cirrhosis
nephrotic syndrome

154
Q

What defines a transudate or an exudate

A

the amount of protein in the fluid

transudate = <30g/L
exudate = >30g/L
155
Q

What is the pathophysiology of an exudate pleural effusion

A

inflammation of the pulmonary capillaries leads to fluids, immune cells and proteins leaking out into the pleural space

156
Q

What causes an exudate pleural effusion

A

infection
malignancy
systemic inflammation - RA, SLE, pancreatitis

157
Q

When is Light’s criteria used?

A

to decide if a pleural effusion is an exudate or a transudate when protein levels are 25-35g/L

158
Q

State Light’s criteria

A

fluid protein:serum protein >0.5

fluid LDH:serium LDH >0.6

fluid LDH > 2/3 normal upper limit serum LDH

159
Q

What are the symptoms of pleural effusion

A

pain on inspiration
SOB
cough

160
Q

What are the signs of pleural effusion

A

dull to percussion
reduced chest expansion
reduced breath sounds
bronchial breathing

161
Q

What investigations should be done in pleural effusion

A

urine dipstick ECG
FBC, U+E, LFTs, CRP
CXR, echo, contrast staging CT if ?malignant
US guided Pleural aspiration

162
Q

What are the signs on CXR of pleural effusion

A

blunting of costophrenic angles

meniscus sign

163
Q

What should the fluid collected on pleural aspiration from pleural effusion be tested for?

A

biochen: protein, LDH, pH
cytology
microbiology
immunology: RF, ANA

164
Q

What is the management of pleural effusion

A

treat the underlying cause

?drain using chest time

165
Q

What can be done for recurrent pleural effusions

A

recurrent aspiration
pleurodesis
indwelling permanant catheter

166
Q

State the pathophysiology of sarcoidosis

A

multisystem granulomatous condition with unknown aetiology

167
Q

Who is sarcioidosis most common in

A

females
20-40y
afro-caribbean

168
Q

What are the features of acute sarcoidosis

A

erythema nodosum
arthralgia
bilateral hilar lymphadenopathy

169
Q

How many cases of acute sarcoidosis resolve spntaneously within a year

A

80%

170
Q

What are the features of chronic sarcoidosis

A

progressive breathlessness
malaise
weight loss

171
Q

What investigation sshould be done in sarcoidosis

A

FBC, ESR, calcium
CXR
transbronchial biopsy

172
Q

What are the blood test findings in sarcoidosis

A

decreased lymphocytes
low platelets
raised ESR
raised calcium - due to abnormal vit D metabolism

173
Q

What are the CXR stages of sarcoidosis

A

0 = no change
1 - BHL
2 - BHL + pulmonary infiltrates’
3 - pulmonary infiltrates, no BHL

174
Q

What is seen on histology in sarciodosis

A

non-caseaeting granulomas

175
Q

What is the treatment of sarciodosis

A

pain relief - NSAIDs if good prognosis (BHL + erythema nodosum)

steroids

chloroquine

176
Q

When are steroids used in teh treatment of sarciodosis

A

if:
stage 2/3 + moderate/severe or progessive symptoms
eye, heart or neurological involvement
raised Calcium

177
Q

What is the stepwise management of paediatric asthma (5-17y) according to NICE

A 
SABA
\+ paed low dose ICS
\+LTRA
\+ LABA
stop LABA, atart MART (paed medium)
increase MART to high dose or start theophylline SR.

Finals (32 decks)

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